Structured Review

R&D Systems icam 1
Change in median levels of serum inflammatory markers over time in patients who received infliximab 3 mg/kg + MTX or placebo + MTX through week 14 with a crossover to infliximab 6 mg/kg + MTX for <t>ICAM-1</t> (A), IL-6 (B), VEGF (C), MMP-3 (D), CRP (E), and IL-12p40 (F) . MTX, methotrexate; ICAM-1, intracellular cell adhesion molecule-1; IL-6, interleukin-6; VEGF, vascular endothelial growth factor; MMP-3, matrix metalloproteinase-3; CRP, C-reactive protein; IL-12p40, interleukin 12.
Icam 1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 99/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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icam 1 - by Bioz Stars, 2020-09
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Images

1) Product Images from "The effect of infliximab plus methotrexate on the modulation of inflammatory disease markers in juvenile idiopathic arthritis: analyses from a randomized, placebo-controlled trial"

Article Title: The effect of infliximab plus methotrexate on the modulation of inflammatory disease markers in juvenile idiopathic arthritis: analyses from a randomized, placebo-controlled trial

Journal: Pediatric Rheumatology Online Journal

doi: 10.1186/1546-0096-8-24

Change in median levels of serum inflammatory markers over time in patients who received infliximab 3 mg/kg + MTX or placebo + MTX through week 14 with a crossover to infliximab 6 mg/kg + MTX for ICAM-1 (A), IL-6 (B), VEGF (C), MMP-3 (D), CRP (E), and IL-12p40 (F) . MTX, methotrexate; ICAM-1, intracellular cell adhesion molecule-1; IL-6, interleukin-6; VEGF, vascular endothelial growth factor; MMP-3, matrix metalloproteinase-3; CRP, C-reactive protein; IL-12p40, interleukin 12.
Figure Legend Snippet: Change in median levels of serum inflammatory markers over time in patients who received infliximab 3 mg/kg + MTX or placebo + MTX through week 14 with a crossover to infliximab 6 mg/kg + MTX for ICAM-1 (A), IL-6 (B), VEGF (C), MMP-3 (D), CRP (E), and IL-12p40 (F) . MTX, methotrexate; ICAM-1, intracellular cell adhesion molecule-1; IL-6, interleukin-6; VEGF, vascular endothelial growth factor; MMP-3, matrix metalloproteinase-3; CRP, C-reactive protein; IL-12p40, interleukin 12.

Techniques Used:

2) Product Images from "Granulocyte-CSF induced inflammation-associated cardiac thrombosis in iron loading mouse heart and can be attenuated by statin therapy"

Article Title: Granulocyte-CSF induced inflammation-associated cardiac thrombosis in iron loading mouse heart and can be attenuated by statin therapy

Journal: Journal of Biomedical Science

doi: 10.1186/1423-0127-18-26

Cardiac mRNA analysis for inflammatory markers and protein analysis for AKT and eNOS expression in I+G mice compared with I+G plus simvastatin treated mice . (A) Total mRNAs were prepared from whole heart tissues, and the levels of ICAM-1, MCP-1, tissue factor, and TNF-alpha transcripts were determined by Quantitative-PCR analysis. Note that the levels of four transcripts, especially of tissue factor and TNF-alpha reduced significantly after simvastatin administration. GADPH expression was used as a control to monitor RNA quality and concentration; **p
Figure Legend Snippet: Cardiac mRNA analysis for inflammatory markers and protein analysis for AKT and eNOS expression in I+G mice compared with I+G plus simvastatin treated mice . (A) Total mRNAs were prepared from whole heart tissues, and the levels of ICAM-1, MCP-1, tissue factor, and TNF-alpha transcripts were determined by Quantitative-PCR analysis. Note that the levels of four transcripts, especially of tissue factor and TNF-alpha reduced significantly after simvastatin administration. GADPH expression was used as a control to monitor RNA quality and concentration; **p

Techniques Used: Expressing, Mouse Assay, Real-time Polymerase Chain Reaction, Concentration Assay

3) Product Images from "CXCR3 Activation Promotes Lymphocyte Transendothelial Migration across Human Hepatic Endothelium under Fluid Flow"

Article Title: CXCR3 Activation Promotes Lymphocyte Transendothelial Migration across Human Hepatic Endothelium under Fluid Flow

Journal: The American Journal of Pathology

doi:

CXCR3 ligands trigger integrin-mediated adhesion of LILs to ICAM-1 and VCAM-1 under static conditions ( A ) and to VCAM-1 under flow ( B ). A: Lymphocytes isolated from chronically inflamed liver samples or matched peripheral blood samples were resuspended to a count of 8 × 10 4 ml and applied to individual wells of an 18-well slide, precoated with ICAM-1 (5 μg/ml). Co-incubation with CXCL9, -10, or -11 significantly increased the binding of LILs, although this effect was abrogated by the addition of pertussis toxin (PTX). Co-incubation of peripheral blood lymphocytes (PBLs) with CXCR3 ligands did not trigger adhesion. Adhesion of LILs and peripheral blood lymphocytes was increased in the presence of the integrin activator MnCl 2 . Data represent mean ± SEM for five replicate experiments. Statistical significance was calculated using paired t -tests, comparing lymphocytes isolated from diseased or normal livers (grouped) with those from the peripheral circulation. B: Adhesion of LILs to immobilized VCAM-1 and ICAM-1 under flow. VCAM-1 or ICAM-1 was immobilized (5 μg/ml) onto glass microslides and adhesion triggered by co-immobilization of the chemokines CXCL9, -10, and -11. CXCL5 was used to control for any nonspecific effects of chemokine co-immobilization because very few lymphocytes express its receptor CXCR2. No adhesion from flow was detected with ICAM-1, even in the presence of CXCR3 ligands. VCAM-1 was able to capture lymphocytes efficiently from flow and co-immobilization of CXCR3 ligands enhanced this effect significantly adhesion being maximal at a chemokine concentration of 400 ng/ml ( P
Figure Legend Snippet: CXCR3 ligands trigger integrin-mediated adhesion of LILs to ICAM-1 and VCAM-1 under static conditions ( A ) and to VCAM-1 under flow ( B ). A: Lymphocytes isolated from chronically inflamed liver samples or matched peripheral blood samples were resuspended to a count of 8 × 10 4 ml and applied to individual wells of an 18-well slide, precoated with ICAM-1 (5 μg/ml). Co-incubation with CXCL9, -10, or -11 significantly increased the binding of LILs, although this effect was abrogated by the addition of pertussis toxin (PTX). Co-incubation of peripheral blood lymphocytes (PBLs) with CXCR3 ligands did not trigger adhesion. Adhesion of LILs and peripheral blood lymphocytes was increased in the presence of the integrin activator MnCl 2 . Data represent mean ± SEM for five replicate experiments. Statistical significance was calculated using paired t -tests, comparing lymphocytes isolated from diseased or normal livers (grouped) with those from the peripheral circulation. B: Adhesion of LILs to immobilized VCAM-1 and ICAM-1 under flow. VCAM-1 or ICAM-1 was immobilized (5 μg/ml) onto glass microslides and adhesion triggered by co-immobilization of the chemokines CXCL9, -10, and -11. CXCL5 was used to control for any nonspecific effects of chemokine co-immobilization because very few lymphocytes express its receptor CXCR2. No adhesion from flow was detected with ICAM-1, even in the presence of CXCR3 ligands. VCAM-1 was able to capture lymphocytes efficiently from flow and co-immobilization of CXCR3 ligands enhanced this effect significantly adhesion being maximal at a chemokine concentration of 400 ng/ml ( P

Techniques Used: Flow Cytometry, Isolation, Incubation, Binding Assay, Concentration Assay

CXCR3 ligands promote lymphocyte adhesion from flow and subsequent transmigration on TNF-α/IFN-γ-stimulated human HSECs. A: Inhibition of CXCR3 with a function blocking antibody or a Gi protein block (PTX) significantly reduces total adhesion of LILs from flow to TNF-α/IFN-γ-stimulated HSECs. Adhesion was further reduced by the addition of blocking antibodies against ICAM-1/VCAM-1. Data represent number of adherent cells per mm 2 per million perfused and are the mean ± SEM of seven experiments. B: Transmigration of adherent lymphocytes through TNF-α/IFN-γ-stimulated HSECs was significantly reduced after CXCR3 and ICAM-1 blockade whereas anti-VCAM-1 mAb had no affect either when used alone or when used in combination. Migrating cells were calculated using frame-by-frame analysis of experimental videos to count the percentage of phase dark (transmigrated) lymphocytes. Data represent paired samples from individual experiments. All experiments were performed at 0.05 Pa.
Figure Legend Snippet: CXCR3 ligands promote lymphocyte adhesion from flow and subsequent transmigration on TNF-α/IFN-γ-stimulated human HSECs. A: Inhibition of CXCR3 with a function blocking antibody or a Gi protein block (PTX) significantly reduces total adhesion of LILs from flow to TNF-α/IFN-γ-stimulated HSECs. Adhesion was further reduced by the addition of blocking antibodies against ICAM-1/VCAM-1. Data represent number of adherent cells per mm 2 per million perfused and are the mean ± SEM of seven experiments. B: Transmigration of adherent lymphocytes through TNF-α/IFN-γ-stimulated HSECs was significantly reduced after CXCR3 and ICAM-1 blockade whereas anti-VCAM-1 mAb had no affect either when used alone or when used in combination. Migrating cells were calculated using frame-by-frame analysis of experimental videos to count the percentage of phase dark (transmigrated) lymphocytes. Data represent paired samples from individual experiments. All experiments were performed at 0.05 Pa.

Techniques Used: Flow Cytometry, Transmigration Assay, Inhibition, Blocking Assay

4) Product Images from "Protective Effects of Luteolin on Lipopolysaccharide-Induced Acute Renal Injury in Mice"

Article Title: Protective Effects of Luteolin on Lipopolysaccharide-Induced Acute Renal Injury in Mice

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

doi: 10.12659/MSM.898177

Effect of luteolin on LPS-induced TNF-α, total NF-κB, p-NF-κB, IL1β, MCP-1 and ICAM-1 protein expressions. Kidneys from mice treated with control buffer, LPS, and LPS plus luteolin were evaluated for protein expressions by ELISA analysis. Data are expressed as mean ±SEM. # P
Figure Legend Snippet: Effect of luteolin on LPS-induced TNF-α, total NF-κB, p-NF-κB, IL1β, MCP-1 and ICAM-1 protein expressions. Kidneys from mice treated with control buffer, LPS, and LPS plus luteolin were evaluated for protein expressions by ELISA analysis. Data are expressed as mean ±SEM. # P

Techniques Used: Mouse Assay, Enzyme-linked Immunosorbent Assay

5) Product Images from "Peroxisome proliferator-activated receptor-? agonists inhibit respiratory syncytial virus-induced expression of intercellular adhesion molecule-1 in human lung epithelial cells"

Article Title: Peroxisome proliferator-activated receptor-? agonists inhibit respiratory syncytial virus-induced expression of intercellular adhesion molecule-1 in human lung epithelial cells

Journal:

doi: 10.1111/j.1365-2567.2006.02539.x

ICAM-1 expression on A549 cells and adhesion of leucocytic cells is dependent on autocrine released IL-1α and TNF-α. Cells were infected with RSV (m.o.i. = 3) and cultured for 36 hr in the presence of blocking antibodies specific for IL-1α
Figure Legend Snippet: ICAM-1 expression on A549 cells and adhesion of leucocytic cells is dependent on autocrine released IL-1α and TNF-α. Cells were infected with RSV (m.o.i. = 3) and cultured for 36 hr in the presence of blocking antibodies specific for IL-1α

Techniques Used: Expressing, Infection, Cell Culture, Blocking Assay

PPAR-γ but not PPAR-α agonists inhibit cell surface expression of ICAM-1 on RSV-infected A549 cells. (a) Cells were pretreated with ciglitazone (5–50 µ m ), troglitazone (5–50 µ m ), 15d-PGJ 2 (5–20 µ
Figure Legend Snippet: PPAR-γ but not PPAR-α agonists inhibit cell surface expression of ICAM-1 on RSV-infected A549 cells. (a) Cells were pretreated with ciglitazone (5–50 µ m ), troglitazone (5–50 µ m ), 15d-PGJ 2 (5–20 µ

Techniques Used: Expressing, Infection

PPAR-γ agonists inhibit RSV-induced cell surface expression of ICAM-1 on NHBE cells. The cells were pretreated with agonists (ciglitazone (20 µ m ), troglitazone (20 µ m ), 15d-PGJ 2 (20 µ m )) for 30 min, infected with RSV (m.o.i.
Figure Legend Snippet: PPAR-γ agonists inhibit RSV-induced cell surface expression of ICAM-1 on NHBE cells. The cells were pretreated with agonists (ciglitazone (20 µ m ), troglitazone (20 µ m ), 15d-PGJ 2 (20 µ m )) for 30 min, infected with RSV (m.o.i.

Techniques Used: Expressing, Infection

PPAR-γ agonists inhibit ICAM-1 mRNA expression in RSV-infected A549 cells. The cellular amount of mRNA encoding for ICAM-1 was quantitatively determined by real-time RT–PCR 24 hr postinfection. (a) Cells were pretreated with ciglitazone
Figure Legend Snippet: PPAR-γ agonists inhibit ICAM-1 mRNA expression in RSV-infected A549 cells. The cellular amount of mRNA encoding for ICAM-1 was quantitatively determined by real-time RT–PCR 24 hr postinfection. (a) Cells were pretreated with ciglitazone

Techniques Used: Expressing, Infection, Quantitative RT-PCR

6) Product Images from "Interleukin-1? Released from Epithelial Cells after Adenovirus Type 37 Infection Activates Intercellular Adhesion Molecule 1 Expression on Human Vascular Endothelial Cells"

Article Title: Interleukin-1? Released from Epithelial Cells after Adenovirus Type 37 Infection Activates Intercellular Adhesion Molecule 1 Expression on Human Vascular Endothelial Cells

Journal: Journal of Virology

doi: 10.1128/JVI.76.1.427-431.2002

ICAM-1 expression on vascular endothelial cells is upregulated after treatment (18 h) with culture supernatants from Ad-infected A549 cells or Ad-infected human corneal epithelial cells. (A) Endothelial ICAM-1 expression after 18-h exposure to culture fluids from Ad-infected A549 cells, mock-infected A549 cells, and medium alone (negative control; NC). (B) Endothelial ICAM-1 expression after 18-h exposure to culture fluids from Ad-infected human corneal epithelial cells, mock-infected A549 cells, and medium alone (negative control; NC). PC, positive control (vascular endothelial cells treated for 18 h with TNF-α [10 U/ml]). Data are from three to nine separate experiments with triplicate samples and are represented as the means ± standard deviations of the means. Significant differences from the mock sample are indicated by * ( P
Figure Legend Snippet: ICAM-1 expression on vascular endothelial cells is upregulated after treatment (18 h) with culture supernatants from Ad-infected A549 cells or Ad-infected human corneal epithelial cells. (A) Endothelial ICAM-1 expression after 18-h exposure to culture fluids from Ad-infected A549 cells, mock-infected A549 cells, and medium alone (negative control; NC). (B) Endothelial ICAM-1 expression after 18-h exposure to culture fluids from Ad-infected human corneal epithelial cells, mock-infected A549 cells, and medium alone (negative control; NC). PC, positive control (vascular endothelial cells treated for 18 h with TNF-α [10 U/ml]). Data are from three to nine separate experiments with triplicate samples and are represented as the means ± standard deviations of the means. Significant differences from the mock sample are indicated by * ( P

Techniques Used: Expressing, Infection, Negative Control, Positive Control

Identification of endothelial ICAM-1-activating factor released from Ad-infected epithelial cells as IL-1α. ICAM-1 expression on vascular endothelial cells after stimulation with culture fluids from Ad-infected (72 h) A549 cells (A), Ad-infected (24 h) corneal epithelial cells (B), or Ad-infected (72 h) corneal epithelial cells (C) is blocked by anti-IL-1α antibody (20 μg/ml) but not by other anticytokine antibodies. Inf, infected cells; Sup, supernatant; NC, negative control (medium alone); PC, positive control (vascular endothelial cells treated for 18 h with TNF-α [10 U/ml]). Data are from three to five separate experiments with triplicate samples and are represented as the means ± standard deviations of the means. Significant differences between antibody-treated and untreated samples are indicated by ** ( P
Figure Legend Snippet: Identification of endothelial ICAM-1-activating factor released from Ad-infected epithelial cells as IL-1α. ICAM-1 expression on vascular endothelial cells after stimulation with culture fluids from Ad-infected (72 h) A549 cells (A), Ad-infected (24 h) corneal epithelial cells (B), or Ad-infected (72 h) corneal epithelial cells (C) is blocked by anti-IL-1α antibody (20 μg/ml) but not by other anticytokine antibodies. Inf, infected cells; Sup, supernatant; NC, negative control (medium alone); PC, positive control (vascular endothelial cells treated for 18 h with TNF-α [10 U/ml]). Data are from three to five separate experiments with triplicate samples and are represented as the means ± standard deviations of the means. Significant differences between antibody-treated and untreated samples are indicated by ** ( P

Techniques Used: Infection, Expressing, Negative Control, Positive Control

ICAM-1 expression on vascular endothelial cells is activated by recombinant cytokines. (A) ICAM-1 expression on endothelial cells incubated for 18 h with IL-1α (4 pg/ml), IL-1β (100 pg/ml), TNF-α (100 U/ml), IL-6 (1 μg/ml), and IL-8 (1 μg/ml). (B) ICAM-1 expression on endothelial cells incubated for 18 h with IL-1α in the presence or absence of anti-IL-1α antibody at the indicated concentration. (C) ICAM-1 expression on endothelial cells incubated for 18 h with IL-1β in the presence or absence of anti-IL-1β antibody at the indicated concentration. (D) ICAM-1 expression on endothelial cells incubated for 18 h with TNF-α in the presence or absence of anti-TNF-α antibody at the indicated concentration. NC, negative control (medium alone); PC, positive control (vascular endothelial cells treated for 18 h with TNF-α [10 U/ml]). Data are from three to six separate experiments with triplicate samples and are represented as the means ± standard deviations of the means. Significant differences between antibody-treated and untreated samples are indicated by * ( P
Figure Legend Snippet: ICAM-1 expression on vascular endothelial cells is activated by recombinant cytokines. (A) ICAM-1 expression on endothelial cells incubated for 18 h with IL-1α (4 pg/ml), IL-1β (100 pg/ml), TNF-α (100 U/ml), IL-6 (1 μg/ml), and IL-8 (1 μg/ml). (B) ICAM-1 expression on endothelial cells incubated for 18 h with IL-1α in the presence or absence of anti-IL-1α antibody at the indicated concentration. (C) ICAM-1 expression on endothelial cells incubated for 18 h with IL-1β in the presence or absence of anti-IL-1β antibody at the indicated concentration. (D) ICAM-1 expression on endothelial cells incubated for 18 h with TNF-α in the presence or absence of anti-TNF-α antibody at the indicated concentration. NC, negative control (medium alone); PC, positive control (vascular endothelial cells treated for 18 h with TNF-α [10 U/ml]). Data are from three to six separate experiments with triplicate samples and are represented as the means ± standard deviations of the means. Significant differences between antibody-treated and untreated samples are indicated by * ( P

Techniques Used: Expressing, Recombinant, Incubation, Concentration Assay, Negative Control, Positive Control

7) Product Images from "Wiskott-Aldrich syndrome protein controls antigen-presenting cell-driven CD4+ T-cell motility by regulating adhesion to intercellular adhesion molecule-1"

Article Title: Wiskott-Aldrich syndrome protein controls antigen-presenting cell-driven CD4+ T-cell motility by regulating adhesion to intercellular adhesion molecule-1

Journal: Immunology

doi: 10.1111/j.1365-2567.2012.03620.x

Wiskott–Aldrich syndrome protein (WASP) -deficient CD4 + T cells elongate on intercellular adhesion molecule 1 (ICAM-1) and immature dendritic cells (iDC). (a) Representative images of green fluorescent protein-positive (GFP + ) short hairpin (sh)
Figure Legend Snippet: Wiskott–Aldrich syndrome protein (WASP) -deficient CD4 + T cells elongate on intercellular adhesion molecule 1 (ICAM-1) and immature dendritic cells (iDC). (a) Representative images of green fluorescent protein-positive (GFP + ) short hairpin (sh)

Techniques Used:

Wiskott–Aldrich syndrome protein (WASP) -deficient CD4 + T cells display an increased adhesion on intercellular adhesion molecule 1 (ICAM-1). (a) Short hairpin (sh) Control and shWASP CD4 + T cells treated or not with blocking anti-lymphocyte function-associated
Figure Legend Snippet: Wiskott–Aldrich syndrome protein (WASP) -deficient CD4 + T cells display an increased adhesion on intercellular adhesion molecule 1 (ICAM-1). (a) Short hairpin (sh) Control and shWASP CD4 + T cells treated or not with blocking anti-lymphocyte function-associated

Techniques Used: Blocking Assay

8) Product Images from "Caveolin-1 Influences LFA-1 Redistribution upon TCR Stimulation in CD8 T Cells"

Article Title: Caveolin-1 Influences LFA-1 Redistribution upon TCR Stimulation in CD8 T Cells

Journal: The Journal of Immunology Author Choice

doi: 10.4049/jimmunol.1700431

Impaired adhesion to ICAM-1 under conditions of fluid shear stress in the absence of Cav1. ( A ) Static adhesion of WT (filled bars) versus Cav1-KO (open bars) CD8 T cells to ICAM-1. CD8 T cells were stimulated with 50 nM PdBu, 1 μg/ml anti-CD3
Figure Legend Snippet: Impaired adhesion to ICAM-1 under conditions of fluid shear stress in the absence of Cav1. ( A ) Static adhesion of WT (filled bars) versus Cav1-KO (open bars) CD8 T cells to ICAM-1. CD8 T cells were stimulated with 50 nM PdBu, 1 μg/ml anti-CD3

Techniques Used:

Absence of Cav1 alters CD8 T cell morphology and polarization upon adhesion to ICAM-1. Cav1-WT and Cav1-KO OT-1 CD8 T cells were allowed to adhere for 30 min to glass slides with and without 3 μg/ml ICAM-1 coating. ( A ) Cells were stained with
Figure Legend Snippet: Absence of Cav1 alters CD8 T cell morphology and polarization upon adhesion to ICAM-1. Cav1-WT and Cav1-KO OT-1 CD8 T cells were allowed to adhere for 30 min to glass slides with and without 3 μg/ml ICAM-1 coating. ( A ) Cells were stained with

Techniques Used: Staining

9) Product Images from "Difference in Th1 and Th17 Lymphocyte Adhesion to Endothelium"

Article Title: Difference in Th1 and Th17 Lymphocyte Adhesion to Endothelium

Journal: Journal of Immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1101647

Expression of adhesion molecules and chemokine receptors on Th17 cells, and their chemokine-dependent interactions with ICAM-1
Figure Legend Snippet: Expression of adhesion molecules and chemokine receptors on Th17 cells, and their chemokine-dependent interactions with ICAM-1

Techniques Used: Expressing

10) Product Images from "Hydrogen Sulfide Alleviates Diabetic Nephropathy in a Streptozotocin-induced Diabetic Rat Model"

Article Title: Hydrogen Sulfide Alleviates Diabetic Nephropathy in a Streptozotocin-induced Diabetic Rat Model

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M114.596593

Concentrations of TNF-α ( A ), MCP-1 ( B ), ICAM-1 ( C ), and VCAM-1 ( D ) in renal tissue measured by ELISA. *, p
Figure Legend Snippet: Concentrations of TNF-α ( A ), MCP-1 ( B ), ICAM-1 ( C ), and VCAM-1 ( D ) in renal tissue measured by ELISA. *, p

Techniques Used: Enzyme-linked Immunosorbent Assay

11) Product Images from "Interleukin-6 Receptor-Mediated Activation of Signal Transducer and Activator of Transcription-3 (STAT3) Promotes Choroidal Neovascularization"

Article Title: Interleukin-6 Receptor-Mediated Activation of Signal Transducer and Activator of Transcription-3 (STAT3) Promotes Choroidal Neovascularization

Journal: The American Journal of Pathology

doi: 10.2353/ajpath.2007.061018

In vivo effects of IL-6R blockade on choroidal expression of inflammatory and angiogenic molecules analyzed by RT-PCR ( A ) and ELISA ( B–D ). IL-6R blockade by the administration of MR16-1 significantly suppressed protein levels of ICAM-1 ( B ), MCP-1 ( C ), and VEGF ( D ). n = 8 to 10. * P
Figure Legend Snippet: In vivo effects of IL-6R blockade on choroidal expression of inflammatory and angiogenic molecules analyzed by RT-PCR ( A ) and ELISA ( B–D ). IL-6R blockade by the administration of MR16-1 significantly suppressed protein levels of ICAM-1 ( B ), MCP-1 ( C ), and VEGF ( D ). n = 8 to 10. * P

Techniques Used: In Vivo, Expressing, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

12) Product Images from "Lung-Targeted Overexpression of the NF-?B Member RelB Inhibits Cigarette Smoke-Induced Inflammation"

Article Title: Lung-Targeted Overexpression of the NF-?B Member RelB Inhibits Cigarette Smoke-Induced Inflammation

Journal: The American Journal of Pathology

doi: 10.1016/j.ajpath.2011.03.030

RelB overexpression reduces cigarette smoke–induced ICAM-1 expression in mouse lungs. Mice were treated with either the RelB or control virus (two doses of 5 × 10 8 plaque-forming units per mouse delivered 24 hours apart) and exposed to
Figure Legend Snippet: RelB overexpression reduces cigarette smoke–induced ICAM-1 expression in mouse lungs. Mice were treated with either the RelB or control virus (two doses of 5 × 10 8 plaque-forming units per mouse delivered 24 hours apart) and exposed to

Techniques Used: Over Expression, Expressing, Mouse Assay

13) Product Images from "Shedding of CD16 disassembles the NK cell immune synapse and boosts serial engagement of target cells"

Article Title: Shedding of CD16 disassembles the NK cell immune synapse and boosts serial engagement of target cells

Journal: The Journal of Cell Biology

doi: 10.1083/jcb.201712085

Expression of a noncleavable form of CD16 leads to prolonged contacts with opsonized target cells. (A and B) NK92/CD16-WT or NK92/CD16-S197P cells were incubated with Daudi-rituximab (Rtx) in 450 × 450 µm 2 microwells. Representative time lapse–enlarged regions show composite fluorescence and brightfield images. NK cells (blue), Daudi-rituximab (green), and dead cells (red) at times indicated. Bars, 20 µm. (A) An NK92/CD16-WT cell (blue) formed a contact with Daudi-rituximab (green; 45 min; yellow arrow). The NK92 cell detached without killing and established a contact with a new target (102 min; white arrow). The second target cell was killed (123 min), and the NK92 cell was detached (156 min). (B) An NK92/CD16-S197P cell formed a contact with a target cell (15 min; yellow arrow) and killed it (36 min). The NK92/CD16-S197P cell died while still attached (387 min). (C) Percentage of NK cell–target interactions that resulted in target cell lysis. (D) Percentage of NK cells that detached by the end of the acquisition. n = 195 interactions from three independent experiments (mean ± SD). (E and F) NK92 cells and transfectants were incubated on surfaces coated with ICAM-1 (−) or ICAM-1 with rituximab for 5 min. Cells were fixed and stained with Alexa Fluor 488–labeled phalloidin marking F-actin. (E) Representative images of spreading on rituximab with ICAM-1. Bars, 20 µm. (F) Percentage of NK92 cells forming dense peripheral rings of F-actin. n = 3 independent experiments (mean ± SD). (G) Representative dot plot assessing the degranulation marker, CD107a, by flow cytometry. NK92 cells and transfectants were activated on ICAM-1 (−) or rituximab with ICAM-1 for 4 h. **, P
Figure Legend Snippet: Expression of a noncleavable form of CD16 leads to prolonged contacts with opsonized target cells. (A and B) NK92/CD16-WT or NK92/CD16-S197P cells were incubated with Daudi-rituximab (Rtx) in 450 × 450 µm 2 microwells. Representative time lapse–enlarged regions show composite fluorescence and brightfield images. NK cells (blue), Daudi-rituximab (green), and dead cells (red) at times indicated. Bars, 20 µm. (A) An NK92/CD16-WT cell (blue) formed a contact with Daudi-rituximab (green; 45 min; yellow arrow). The NK92 cell detached without killing and established a contact with a new target (102 min; white arrow). The second target cell was killed (123 min), and the NK92 cell was detached (156 min). (B) An NK92/CD16-S197P cell formed a contact with a target cell (15 min; yellow arrow) and killed it (36 min). The NK92/CD16-S197P cell died while still attached (387 min). (C) Percentage of NK cell–target interactions that resulted in target cell lysis. (D) Percentage of NK cells that detached by the end of the acquisition. n = 195 interactions from three independent experiments (mean ± SD). (E and F) NK92 cells and transfectants were incubated on surfaces coated with ICAM-1 (−) or ICAM-1 with rituximab for 5 min. Cells were fixed and stained with Alexa Fluor 488–labeled phalloidin marking F-actin. (E) Representative images of spreading on rituximab with ICAM-1. Bars, 20 µm. (F) Percentage of NK92 cells forming dense peripheral rings of F-actin. n = 3 independent experiments (mean ± SD). (G) Representative dot plot assessing the degranulation marker, CD107a, by flow cytometry. NK92 cells and transfectants were activated on ICAM-1 (−) or rituximab with ICAM-1 for 4 h. **, P

Techniques Used: Expressing, Incubation, Fluorescence, Lysis, Staining, Labeling, Marker, Flow Cytometry, Cytometry

Expression of a noncleavable form of CD16 prevents reduction of perforin in sequential stimulation. (A) Schematic representation of CD16-WT and CD16-S197P indicating a single point mutation, S197P, which renders CD16 insensitive to ADAM17. (B) The NK92 cell line was transduced to express CD16-WT or CD16-S197P. Representative histograms of surface CD16 on parental cell line (gray) and NK92/CD16-WT or NK92/CD16-S197P before (black) and after activation with Daudi-rituximab (Rtx; red) or PMA/ionomycin (orange). The same histogram for a parental cell line is shown in both panels. (C) CD16 expression levels normalized to unstimulated (US) CD16 + cells ( n = 5 independent experiments; mean ± SD). (D and E) Transfected NK92 cells were sequentially activated through CD16 on slides coated with rituximab and ICAM-1. Secreted perforin was captured with anti-perforin mAb and visualized by a noncompeting Alexa Fluor 488–labeled anti-perforin mAb. Median fluorescence of perforin for NK92/CD16-WT (D) or NK92/CD16-S197P (E). n = 7; mean ± SEM; symbols represent different experiments. **, P
Figure Legend Snippet: Expression of a noncleavable form of CD16 prevents reduction of perforin in sequential stimulation. (A) Schematic representation of CD16-WT and CD16-S197P indicating a single point mutation, S197P, which renders CD16 insensitive to ADAM17. (B) The NK92 cell line was transduced to express CD16-WT or CD16-S197P. Representative histograms of surface CD16 on parental cell line (gray) and NK92/CD16-WT or NK92/CD16-S197P before (black) and after activation with Daudi-rituximab (Rtx; red) or PMA/ionomycin (orange). The same histogram for a parental cell line is shown in both panels. (C) CD16 expression levels normalized to unstimulated (US) CD16 + cells ( n = 5 independent experiments; mean ± SD). (D and E) Transfected NK92 cells were sequentially activated through CD16 on slides coated with rituximab and ICAM-1. Secreted perforin was captured with anti-perforin mAb and visualized by a noncompeting Alexa Fluor 488–labeled anti-perforin mAb. Median fluorescence of perforin for NK92/CD16-WT (D) or NK92/CD16-S197P (E). n = 7; mean ± SEM; symbols represent different experiments. **, P

Techniques Used: Expressing, Mutagenesis, Activation Assay, Transfection, Labeling, Fluorescence

Effective restimulation of NK cells is receptor dependent. (A–I) NK cells were sequentially activated through CD16 and NKG2D on slides coated with either rituximab (Rtx) or MICA and both with ICAM-1. Slides were also coated with anti-perforin mAb to capture secreted perforin, which was visualized by a noncompeting Alexa Fluor 488–labeled anti-perforin mAb. (A) Schematic representation of experimental approach. NK cells were sequentially incubated for 1 h on differently coated surfaces as indicated. (B) Representative images of perforin secreted from one cell during sequential stimulations. Bars, 10 µm. (C and F) Quantitative analysis of perforin secreted by cells from a representative donor. Each point is the integrated fluorescence intensity (IFI) of perforin captured from one cell (median ± interquartile range [IQR]). (D and G) Median IFI values of perforin secretion from different donors ( n = 6; mean ± SEM; symbols represent different donors). (E and H) Intracellular (IC) perforin levels were assessed by flow cytometry upon each round of stimulation. Graphs represent geometric mean fluorescence intensity (gMFI) values ( n = 3; mean ± SD; symbols represent different donors). (I) Comparison of gMFI values of intracellular perforin upon two rounds of stimulation on either rituximab or MICA. *, P
Figure Legend Snippet: Effective restimulation of NK cells is receptor dependent. (A–I) NK cells were sequentially activated through CD16 and NKG2D on slides coated with either rituximab (Rtx) or MICA and both with ICAM-1. Slides were also coated with anti-perforin mAb to capture secreted perforin, which was visualized by a noncompeting Alexa Fluor 488–labeled anti-perforin mAb. (A) Schematic representation of experimental approach. NK cells were sequentially incubated for 1 h on differently coated surfaces as indicated. (B) Representative images of perforin secreted from one cell during sequential stimulations. Bars, 10 µm. (C and F) Quantitative analysis of perforin secreted by cells from a representative donor. Each point is the integrated fluorescence intensity (IFI) of perforin captured from one cell (median ± interquartile range [IQR]). (D and G) Median IFI values of perforin secretion from different donors ( n = 6; mean ± SEM; symbols represent different donors). (E and H) Intracellular (IC) perforin levels were assessed by flow cytometry upon each round of stimulation. Graphs represent geometric mean fluorescence intensity (gMFI) values ( n = 3; mean ± SD; symbols represent different donors). (I) Comparison of gMFI values of intracellular perforin upon two rounds of stimulation on either rituximab or MICA. *, P

Techniques Used: Labeling, Incubation, Fluorescence, Flow Cytometry, Cytometry

Activation via CD16 triggers the assembly of a cytolytic kinapse. (A) NK cells were incubated for 5 min on slides coated with rituximab (Rtx) or MICA, both with ICAM-1, or ICAM-1 alone (−) and then fixed. Panels show representative confocal images of F-actin stained with Alexa Fluor 488–labeled phalloidin. (B) Cells were scored according to their F-actin distribution; dense symmetrical rings (gray) accumulated asymmetrically at the leading edge (yellow) or more evenly distributed across the interface (green). n = 3 independent experiments. (C) IRM live-cell imaging of the contact between NK cells and glass slides coated with rituximab or MICA, both with ICAM-1. An overlay of all 360 frames (6 min at one frame per second) is shown colored according to time. Bars, 20 µm. (D and E) Surface area (D) and circularity (E) of cells was analyzed. Circularity values approaching 1 indicate a more circular shape, whereas 0 indicates an elongated shape ( n = 3 independent experiments; mean ± SEM). (F) NK cell motility on activating surfaces. NK cells were labeled with Calcein and allowed to settle on surfaces coated with ICAM-1 alone (−), rituximab, or MICA, both with ICAM-1 ±1 µM TAPI-0 (where indicated). Images were acquired every 30 s for 45 min, and cells were tracked using Cell Tracker, a MATLAB plugin. n = 20 individual cell tracks from one representative donor. Axes are ±300 µm. (G) Speed of NK cells on differently coated surfaces. Each point represents the average speed of an individual cell from a representative donor (median ± IQR). (H) Mean NK cell speed ( n = 4 different donors; mean ± SEM). *, P
Figure Legend Snippet: Activation via CD16 triggers the assembly of a cytolytic kinapse. (A) NK cells were incubated for 5 min on slides coated with rituximab (Rtx) or MICA, both with ICAM-1, or ICAM-1 alone (−) and then fixed. Panels show representative confocal images of F-actin stained with Alexa Fluor 488–labeled phalloidin. (B) Cells were scored according to their F-actin distribution; dense symmetrical rings (gray) accumulated asymmetrically at the leading edge (yellow) or more evenly distributed across the interface (green). n = 3 independent experiments. (C) IRM live-cell imaging of the contact between NK cells and glass slides coated with rituximab or MICA, both with ICAM-1. An overlay of all 360 frames (6 min at one frame per second) is shown colored according to time. Bars, 20 µm. (D and E) Surface area (D) and circularity (E) of cells was analyzed. Circularity values approaching 1 indicate a more circular shape, whereas 0 indicates an elongated shape ( n = 3 independent experiments; mean ± SEM). (F) NK cell motility on activating surfaces. NK cells were labeled with Calcein and allowed to settle on surfaces coated with ICAM-1 alone (−), rituximab, or MICA, both with ICAM-1 ±1 µM TAPI-0 (where indicated). Images were acquired every 30 s for 45 min, and cells were tracked using Cell Tracker, a MATLAB plugin. n = 20 individual cell tracks from one representative donor. Axes are ±300 µm. (G) Speed of NK cells on differently coated surfaces. Each point represents the average speed of an individual cell from a representative donor (median ± IQR). (H) Mean NK cell speed ( n = 4 different donors; mean ± SEM). *, P

Techniques Used: Activation Assay, Incubation, Staining, Labeling, Live Cell Imaging

14) Product Images from "Autophagy protein ATG7 is a critical regulator of endothelial cell inflammation and permeability"

Article Title: Autophagy protein ATG7 is a critical regulator of endothelial cell inflammation and permeability

Journal: Scientific Reports

doi: 10.1038/s41598-020-70126-7

ATG7 knockdown inhibits thrombin-mediated expression of inflammatory proteins and NF-κB activity. HPAEC were transfected with si-Con or si-ATG7 for 48 h and then treated with thrombin (5 U/ml) for 6 h. ( A , B ) Conditioned media was collected from the cells and ELISAs were performed for ( A ) IL-6, ( B ) MCP-1. Error bars represent mean ± S.E. (n = 5 for each condition). ( C D ) Cell lysates were analyzed by ELISA for ( C ) ICAM-1 and ( D ) VCAM-1 levels. Error bars represent mean ± S.E. (n = 5 for each condition). ( E ) HPAEC were transfected with si-Con or si-ATG7 for 24 h, then transfected with NF-κBLUC and Renilla LUC constructs as described in the “ Materials and Methods ”. The cells were then treated with thrombin (5 U/ml) for 6 h and cell extracts were assayed for Firefly and Renilla luciferase activities. Renilla luciferase was used as an internal control for transfection efficiency. Error bars represent mean ± S.E. (n = 6 for each condition).
Figure Legend Snippet: ATG7 knockdown inhibits thrombin-mediated expression of inflammatory proteins and NF-κB activity. HPAEC were transfected with si-Con or si-ATG7 for 48 h and then treated with thrombin (5 U/ml) for 6 h. ( A , B ) Conditioned media was collected from the cells and ELISAs were performed for ( A ) IL-6, ( B ) MCP-1. Error bars represent mean ± S.E. (n = 5 for each condition). ( C D ) Cell lysates were analyzed by ELISA for ( C ) ICAM-1 and ( D ) VCAM-1 levels. Error bars represent mean ± S.E. (n = 5 for each condition). ( E ) HPAEC were transfected with si-Con or si-ATG7 for 24 h, then transfected with NF-κBLUC and Renilla LUC constructs as described in the “ Materials and Methods ”. The cells were then treated with thrombin (5 U/ml) for 6 h and cell extracts were assayed for Firefly and Renilla luciferase activities. Renilla luciferase was used as an internal control for transfection efficiency. Error bars represent mean ± S.E. (n = 6 for each condition).

Techniques Used: Expressing, Activity Assay, Transfection, Enzyme-linked Immunosorbent Assay, Construct, Luciferase

15) Product Images from "Evaluation of the topographical influence on the cellular behavior of human umbilical vein endothelial cells"

Article Title: Evaluation of the topographical influence on the cellular behavior of human umbilical vein endothelial cells

Journal: Advanced biosystems

doi: 10.1002/adbi.201700217

Comparison of representative immunofluorescence images and quantified values of cell markers expression of HUVEC monolayer on selected patterned substrates. (A) CD31 expression (Red) of HUVEC monolayer on selected patterned substrates. (B) VE-cadherin expression (Green) of HUVEC monolayer on selected patterned substrates. (C) ICAM-1 expression (Red) of HUVEC monolayer on selected patterned substrates. Due to the uneven expression of ICAM-1 on the HUVEC monolayers, DAPI stained nuclei (Blue) was showed with ICAM-1 to help confirm the monolayer. In all panels, white bar represents 100 μm. Data (n=15 for all surfaces) were evaluated on outliers using Grubb’s test. Statistical analysis was performed using one-way ANOVA test with Tukey’s post-hoc test. Data represent mean±SD, *P≤0.05, **P≤0.01, ***P≤0.001, ****P≤0.0001.
Figure Legend Snippet: Comparison of representative immunofluorescence images and quantified values of cell markers expression of HUVEC monolayer on selected patterned substrates. (A) CD31 expression (Red) of HUVEC monolayer on selected patterned substrates. (B) VE-cadherin expression (Green) of HUVEC monolayer on selected patterned substrates. (C) ICAM-1 expression (Red) of HUVEC monolayer on selected patterned substrates. Due to the uneven expression of ICAM-1 on the HUVEC monolayers, DAPI stained nuclei (Blue) was showed with ICAM-1 to help confirm the monolayer. In all panels, white bar represents 100 μm. Data (n=15 for all surfaces) were evaluated on outliers using Grubb’s test. Statistical analysis was performed using one-way ANOVA test with Tukey’s post-hoc test. Data represent mean±SD, *P≤0.05, **P≤0.01, ***P≤0.001, ****P≤0.0001.

Techniques Used: Immunofluorescence, Expressing, Staining

16) Product Images from "Inhibition of Protein Kinase C Delta Attenuates Allergic Airway Inflammation through Suppression of PI3K/Akt/mTOR/HIF-1 Alpha/VEGF Pathway"

Article Title: Inhibition of Protein Kinase C Delta Attenuates Allergic Airway Inflammation through Suppression of PI3K/Akt/mTOR/HIF-1 Alpha/VEGF Pathway

Journal: PLoS ONE

doi: 10.1371/journal.pone.0081773

Effect of rottlerin, LY294002, or rapamycin on eotaxin, ICAM-1, and VCAM-1 levels in OVA-inhaled mice. (A) Western blotting of eotaxin, ICAM-1, and VCAM-1 in lung tissues. (B) Densitometric analyses are presented as the relative ratio of each molecule to actin. The relative ratio of each molecule in the lung tissues of SAL+SAL mice is arbitrarily presented as 1. (C) The levels of eotaxin, ICAM-1, and VCAM-1 were quantified by ELISA. The protein expression of these adhesion molecules was measured at 48 h after the last challenge in mice. Results from four independent experiments with 5 mice/group are given as mean ± SEM. # p
Figure Legend Snippet: Effect of rottlerin, LY294002, or rapamycin on eotaxin, ICAM-1, and VCAM-1 levels in OVA-inhaled mice. (A) Western blotting of eotaxin, ICAM-1, and VCAM-1 in lung tissues. (B) Densitometric analyses are presented as the relative ratio of each molecule to actin. The relative ratio of each molecule in the lung tissues of SAL+SAL mice is arbitrarily presented as 1. (C) The levels of eotaxin, ICAM-1, and VCAM-1 were quantified by ELISA. The protein expression of these adhesion molecules was measured at 48 h after the last challenge in mice. Results from four independent experiments with 5 mice/group are given as mean ± SEM. # p

Techniques Used: Mouse Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing

17) Product Images from "JAK tyrosine kinases promote hierarchical activation of Rho and Rap modules of integrin activation"

Article Title: JAK tyrosine kinases promote hierarchical activation of Rho and Rap modules of integrin activation

Journal: The Journal of Cell Biology

doi: 10.1083/jcb.201303067

JAK2 and JAK3 regulate CXCL12-triggered underflow arrest on ICAM-1 and homing to secondary lymphoid organs of human primary T lymphocytes. Underflow adhesion assays. (A) Lymphocytes were treated with buffer (control), DMSO (vehicle), or 100 µM AG490 for 1 h; three experiments. Error bars show SDs. *, P
Figure Legend Snippet: JAK2 and JAK3 regulate CXCL12-triggered underflow arrest on ICAM-1 and homing to secondary lymphoid organs of human primary T lymphocytes. Underflow adhesion assays. (A) Lymphocytes were treated with buffer (control), DMSO (vehicle), or 100 µM AG490 for 1 h; three experiments. Error bars show SDs. *, P

Techniques Used:

JAK2 and JAK3 control CXCL12-triggered LFA-1–mediated static adhesion to ICAM-1 of human primary T lymphocytes. (A) Effect of JAK inhibitors on JAK2 and JAK3 activation. Lymphocytes were treated with buffer (NT and control), 100 µM AG490, 40 µM P1-TKIP, or 200 µM WHI-P154 for 1 h and stimulated with 0.2 µM CXCL12 for 60 s. Lysates were immunoprecipitated with antiphosphotyrosine antibody and probed with anti-JAK2 (left) or anti-JAK3 antibody (right). The expression level of each protein was assessed in whole-cell lysates with anti-JAK2 or anti-JAK3 antibodies; representative experiment of three. (B) Quantification of immunoreactive bands. The relative ratio of the band intensity of phospho-JAK2 (left) and phospho-JAK3 (right) was normalized to the level of NT intensity. Mean values of three experiments for each protein. *, P
Figure Legend Snippet: JAK2 and JAK3 control CXCL12-triggered LFA-1–mediated static adhesion to ICAM-1 of human primary T lymphocytes. (A) Effect of JAK inhibitors on JAK2 and JAK3 activation. Lymphocytes were treated with buffer (NT and control), 100 µM AG490, 40 µM P1-TKIP, or 200 µM WHI-P154 for 1 h and stimulated with 0.2 µM CXCL12 for 60 s. Lysates were immunoprecipitated with antiphosphotyrosine antibody and probed with anti-JAK2 (left) or anti-JAK3 antibody (right). The expression level of each protein was assessed in whole-cell lysates with anti-JAK2 or anti-JAK3 antibodies; representative experiment of three. (B) Quantification of immunoreactive bands. The relative ratio of the band intensity of phospho-JAK2 (left) and phospho-JAK3 (right) was normalized to the level of NT intensity. Mean values of three experiments for each protein. *, P

Techniques Used: Activation Assay, Immunoprecipitation, Expressing

Human primary T lymphocytes lacking of JAK2 or JAK3 display reduced CXCL12-triggered adhesion to ICAM-1. (A) Immunoblot evaluation of JAK2 and JAK3 expression; lymphocytes were electroporated with a pool of four scrambled or JAK2 (left)- or JAK3 (right)-specific siRNAs and kept in culture for 24 h. Shown is the protein content compared with actin. The expression level of each protein was assessed in whole-cell lysates with anti-JAK2 or anti-JAK3 antibodies and then with an antiactin antibody for the loading control; representative experiment of five. (B) Quantification of immunoreactive bands. The relative ratio of the band intensity of total JAK2 (left) and JAK3 (right) was normalized to the level of NT intensity. Mean values of five experiments. (C) Flow cytometry measurement of CXCR4 (left) and CD18 (right) expression. Lymphocytes were treated as described in A; five experiments. (D) Static adhesion assay to ICAM-1. Lymphocytes were treated as in A and stimulated with buffer (no) or 0.2 µM CXCL12 (agonist); five experiments in triplicate. Error bars show SDs. *, P
Figure Legend Snippet: Human primary T lymphocytes lacking of JAK2 or JAK3 display reduced CXCL12-triggered adhesion to ICAM-1. (A) Immunoblot evaluation of JAK2 and JAK3 expression; lymphocytes were electroporated with a pool of four scrambled or JAK2 (left)- or JAK3 (right)-specific siRNAs and kept in culture for 24 h. Shown is the protein content compared with actin. The expression level of each protein was assessed in whole-cell lysates with anti-JAK2 or anti-JAK3 antibodies and then with an antiactin antibody for the loading control; representative experiment of five. (B) Quantification of immunoreactive bands. The relative ratio of the band intensity of total JAK2 (left) and JAK3 (right) was normalized to the level of NT intensity. Mean values of five experiments. (C) Flow cytometry measurement of CXCR4 (left) and CD18 (right) expression. Lymphocytes were treated as described in A; five experiments. (D) Static adhesion assay to ICAM-1. Lymphocytes were treated as in A and stimulated with buffer (no) or 0.2 µM CXCL12 (agonist); five experiments in triplicate. Error bars show SDs. *, P

Techniques Used: Expressing, Flow Cytometry, Cytometry, Cell Adhesion Assay

Heterotrimeric Gα i protein signaling is differently involved in Rap1A, RhoA, and Rac1 activation by CXCL12. (A) Static adhesion assay to ICAM-1. Lymphocytes were treated with buffer (not treated [NT]) or 2 µg/ml pertussis toxin (PTx) for 2 h and stimulated with 0.2 µM CXCL12 (agonist); four experiments in triplicate. (B, left) Rap1A activation was measured by pull-down assay. Lymphocytes were treated as in A and stimulated with 0.2 µM CXCL12; representative experiment of three. (right) The relative ratio of the band intensity of GTP-Rap1A was normalized to the level of total Rap1A intensity. (C and D) G-LISA assay detecting RhoA (C) and Rac1 (D) activation. Lymphocytes were treated as in A and stimulated with 0.2 µM CXCL12 (agonist). The percentage of fold increase of the RhoA and Rac1 activation was normalized to the level of NT intensity; mean of three experiments. Error bars show SDs. *, P
Figure Legend Snippet: Heterotrimeric Gα i protein signaling is differently involved in Rap1A, RhoA, and Rac1 activation by CXCL12. (A) Static adhesion assay to ICAM-1. Lymphocytes were treated with buffer (not treated [NT]) or 2 µg/ml pertussis toxin (PTx) for 2 h and stimulated with 0.2 µM CXCL12 (agonist); four experiments in triplicate. (B, left) Rap1A activation was measured by pull-down assay. Lymphocytes were treated as in A and stimulated with 0.2 µM CXCL12; representative experiment of three. (right) The relative ratio of the band intensity of GTP-Rap1A was normalized to the level of total Rap1A intensity. (C and D) G-LISA assay detecting RhoA (C) and Rac1 (D) activation. Lymphocytes were treated as in A and stimulated with 0.2 µM CXCL12 (agonist). The percentage of fold increase of the RhoA and Rac1 activation was normalized to the level of NT intensity; mean of three experiments. Error bars show SDs. *, P

Techniques Used: Activation Assay, Cell Adhesion Assay, Pull Down Assay

18) Product Images from "Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue"

Article Title: Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue

Journal: Clinical and Developmental Immunology

doi: 10.1155/2013/617809

Del-1 inhibits ICAM-1-dependent chemokine production by neutrophils. (a)–(c) ATRA-differentiated HL-60 neutrophils were cultured for 24 hours on plates coated with Fc protein control, ICAM-1-Fc, or Del-1-Fc, and induction of release of CCL3 (a), CXCL2 (b), and TNF (c) was assayed by ELISA. (d)-(e) ATRA-differentiated HL-60 neutrophils were cultured for 24 hours on ICAM-1-Fc-coated plates in the presence of the indicated concentrations of soluble Del-1, and induction of release of CCL3 (d) and CXCL2 (e) was assayed by ELISA. (f)-(g) ATRA-differentiated HL-60 neutrophils were stimulated for 24 hours with 1 μ g/mL Pam 3 CSK 4 or 0.1 μ g/mL LPS, in the absence or presence of the indicated concentrations of Del-1, and induction of release of CCL3 (f) and CXCL2 (g) was assayed by ELISA. Data are means ± SD ((a)–(e), n ≥ 4 and (f)-(g), n = 2 sets of HL-60 cells). * P
Figure Legend Snippet: Del-1 inhibits ICAM-1-dependent chemokine production by neutrophils. (a)–(c) ATRA-differentiated HL-60 neutrophils were cultured for 24 hours on plates coated with Fc protein control, ICAM-1-Fc, or Del-1-Fc, and induction of release of CCL3 (a), CXCL2 (b), and TNF (c) was assayed by ELISA. (d)-(e) ATRA-differentiated HL-60 neutrophils were cultured for 24 hours on ICAM-1-Fc-coated plates in the presence of the indicated concentrations of soluble Del-1, and induction of release of CCL3 (d) and CXCL2 (e) was assayed by ELISA. (f)-(g) ATRA-differentiated HL-60 neutrophils were stimulated for 24 hours with 1 μ g/mL Pam 3 CSK 4 or 0.1 μ g/mL LPS, in the absence or presence of the indicated concentrations of Del-1, and induction of release of CCL3 (f) and CXCL2 (g) was assayed by ELISA. Data are means ± SD ((a)–(e), n ≥ 4 and (f)-(g), n = 2 sets of HL-60 cells). * P

Techniques Used: Cell Culture, Enzyme-linked Immunosorbent Assay

Regulation of Del-1 versus ICAM-1 and VCAM-1 by inflammatory stimuli. HUVEC were cultured for the indicated time intervals with 10 ng/mL TNF (a), 5 μ g/mL serum amyloid A (SAA; (b)), P. gingivalis (Pg; MOI = 10 : 1) (c), Pam 3 CSK 4 or LPS (both at 0.5 μ g/mL; (d)), 10 ng/mL IFN γ (e), or IL-17A or IL-17F (both at 10 ng/mL; (f)) and assayed for Del-1, ICAM-1, and VCAM-1 mRNA expression. Results were normalized to those of GAPDH mRNA and expressed as fold change in transcript levels relative to those of medium-treated cells at 2 hours (HRS), the average value of which was taken as 1. The medium-treated groups in (b) and (c) are the same (SAA and Pg were tested together but were separated in the graphs for enhanced clarity). Data are means ± SD of duplicate determinations from one of three independent sets of experiments that yielded similar results.
Figure Legend Snippet: Regulation of Del-1 versus ICAM-1 and VCAM-1 by inflammatory stimuli. HUVEC were cultured for the indicated time intervals with 10 ng/mL TNF (a), 5 μ g/mL serum amyloid A (SAA; (b)), P. gingivalis (Pg; MOI = 10 : 1) (c), Pam 3 CSK 4 or LPS (both at 0.5 μ g/mL; (d)), 10 ng/mL IFN γ (e), or IL-17A or IL-17F (both at 10 ng/mL; (f)) and assayed for Del-1, ICAM-1, and VCAM-1 mRNA expression. Results were normalized to those of GAPDH mRNA and expressed as fold change in transcript levels relative to those of medium-treated cells at 2 hours (HRS), the average value of which was taken as 1. The medium-treated groups in (b) and (c) are the same (SAA and Pg were tested together but were separated in the graphs for enhanced clarity). Data are means ± SD of duplicate determinations from one of three independent sets of experiments that yielded similar results.

Techniques Used: Cell Culture, Expressing

Expression of endothelial adhesion molecules in Del-1 deficiency. (a) Gingiva dissected from 16-week-old C57BL/6 Edil 3 +/+ (WT) and Edil 3 −/− mice were processed for quantitative real-time PCR analysis of mRNA expression of the indicated genes; results were normalized to those of GAPDH mRNA and expressed as fold change in Edil 3 −/− transcript levels relative to WT, the average value of which was taken as 1. (b) Sagittal sections of interdental gingiva from 16-week-old C57BL/6 WT or Edil 3 −/− mice were stained for ICAM-1, VCAM-1, or E-selectin and CD31, as indicated. Shown are representative overlays of differential interference contrast and fluorescent confocal images, with colocalization demonstrated in merged images (scale bar, 50 μ m). (c) The fluorescence intensities of the images shown here and of additional representative images from independent mice (5 per group) were quantified using ImageJ analysis. In (a) and (c), data are means ± SD ( n = 5 mice per group). No statistically significant differences were detected between Edil 3 −/− and WT littermate controls.
Figure Legend Snippet: Expression of endothelial adhesion molecules in Del-1 deficiency. (a) Gingiva dissected from 16-week-old C57BL/6 Edil 3 +/+ (WT) and Edil 3 −/− mice were processed for quantitative real-time PCR analysis of mRNA expression of the indicated genes; results were normalized to those of GAPDH mRNA and expressed as fold change in Edil 3 −/− transcript levels relative to WT, the average value of which was taken as 1. (b) Sagittal sections of interdental gingiva from 16-week-old C57BL/6 WT or Edil 3 −/− mice were stained for ICAM-1, VCAM-1, or E-selectin and CD31, as indicated. Shown are representative overlays of differential interference contrast and fluorescent confocal images, with colocalization demonstrated in merged images (scale bar, 50 μ m). (c) The fluorescence intensities of the images shown here and of additional representative images from independent mice (5 per group) were quantified using ImageJ analysis. In (a) and (c), data are means ± SD ( n = 5 mice per group). No statistically significant differences were detected between Edil 3 −/− and WT littermate controls.

Techniques Used: Expressing, Mouse Assay, Real-time Polymerase Chain Reaction, Staining, Fluorescence

19) Product Images from "Regulation of Endothelial Cell Adhesion Molecule Expression by Mast Cells, Macrophages, and Neutrophils"

Article Title: Regulation of Endothelial Cell Adhesion Molecule Expression by Mast Cells, Macrophages, and Neutrophils

Journal: PLoS ONE

doi: 10.1371/journal.pone.0014525

Adhesion molecule protein levels from MHEC treated with different degranulated mast cell supernatants. Commercial ELISA kits were used to determine VCAM-1, ICAM-1, P-selectin, and E-selectin in MHEC lysate. Degranulated mast cell supernatants from different mice, as indicated, were used to treat mouse MHEC for 24 hours. Data are presented as mean ± SE of three independent experiments. P
Figure Legend Snippet: Adhesion molecule protein levels from MHEC treated with different degranulated mast cell supernatants. Commercial ELISA kits were used to determine VCAM-1, ICAM-1, P-selectin, and E-selectin in MHEC lysate. Degranulated mast cell supernatants from different mice, as indicated, were used to treat mouse MHEC for 24 hours. Data are presented as mean ± SE of three independent experiments. P

Techniques Used: Enzyme-linked Immunosorbent Assay, Mouse Assay

Adhesion molecule expression in MHEC after neutrophil stimulation. Neutrophil lysates were prepared from bone marrow from different mice, as indicated, and used to induce MHEC for four hours. VCAM-1 ( A ), ICAM-1 ( B ), P-selectin ( C ), and E-selectin ( D ) mRNA levels were quantified by RT-PCR and normalized to β-actin. Fold changes were determined relative to unstimulated MHEC. ELISA determined VCAM-1 ( E ) and E-selectin ( F ) protein levels in lysates of MHEC that were stimulated with neutrophil lysates from different mice, as indicated, for 24 hours. Data were presented as mean ± SE of three to six independent experiments. P
Figure Legend Snippet: Adhesion molecule expression in MHEC after neutrophil stimulation. Neutrophil lysates were prepared from bone marrow from different mice, as indicated, and used to induce MHEC for four hours. VCAM-1 ( A ), ICAM-1 ( B ), P-selectin ( C ), and E-selectin ( D ) mRNA levels were quantified by RT-PCR and normalized to β-actin. Fold changes were determined relative to unstimulated MHEC. ELISA determined VCAM-1 ( E ) and E-selectin ( F ) protein levels in lysates of MHEC that were stimulated with neutrophil lysates from different mice, as indicated, for 24 hours. Data were presented as mean ± SE of three to six independent experiments. P

Techniques Used: Expressing, Mouse Assay, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

Adhesion molecule expression in MHEC after macrophage stimulation. MHEC were treated with macrophage cell lysates from different mice, as indicated, for four hours. VCAM-1 ( A ), ICAM-1 ( B ), P-selectin ( C ), and E-selectin ( D ) mRNA levels were quantified by RT-PCR and normalized to β-actin. Fold changes were calculated relative to unstimulated EC. ELISA determined VCAM-1 ( E ) and E-selectin ( F ) protein levels in lysates of MHEC that were stimulated with macrophage lysates from different mice for 24 hours. Data were presented as mean ± SE of three to six independent experiments. P
Figure Legend Snippet: Adhesion molecule expression in MHEC after macrophage stimulation. MHEC were treated with macrophage cell lysates from different mice, as indicated, for four hours. VCAM-1 ( A ), ICAM-1 ( B ), P-selectin ( C ), and E-selectin ( D ) mRNA levels were quantified by RT-PCR and normalized to β-actin. Fold changes were calculated relative to unstimulated EC. ELISA determined VCAM-1 ( E ) and E-selectin ( F ) protein levels in lysates of MHEC that were stimulated with macrophage lysates from different mice for 24 hours. Data were presented as mean ± SE of three to six independent experiments. P

Techniques Used: Expressing, Mouse Assay, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

Degranulated mast cells induced MHEC adhesion molecule expression. RT-PCR determined VCAM-1 (A), ICAM-1 (B), P-selectin (C), E-selectin (D), ICAM-1 (E), and P-selectin ( F ) mRNA levels relative to β-actin in MHEC after stimulation with conditioned media of mast cells from WT and different cytokine-deficient mice, or WT mast cell conditioned media pre-treated with anti-mouse TNF-α antibody or isotype control IgG (R D Systems). Fold change was calculated relative to unstimulated MHEC. Data were presented as mean ± SE of three independent experiments. P
Figure Legend Snippet: Degranulated mast cells induced MHEC adhesion molecule expression. RT-PCR determined VCAM-1 (A), ICAM-1 (B), P-selectin (C), E-selectin (D), ICAM-1 (E), and P-selectin ( F ) mRNA levels relative to β-actin in MHEC after stimulation with conditioned media of mast cells from WT and different cytokine-deficient mice, or WT mast cell conditioned media pre-treated with anti-mouse TNF-α antibody or isotype control IgG (R D Systems). Fold change was calculated relative to unstimulated MHEC. Data were presented as mean ± SE of three independent experiments. P

Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Mouse Assay

20) Product Images from "Caveolin-1 Influences LFA-1 Redistribution upon TCR Stimulation in CD8 T Cells"

Article Title: Caveolin-1 Influences LFA-1 Redistribution upon TCR Stimulation in CD8 T Cells

Journal: The Journal of Immunology Author Choice

doi: 10.4049/jimmunol.1700431

Impaired adhesion to ICAM-1 under conditions of fluid shear stress in the absence of Cav1. ( A ) Static adhesion of WT (filled bars) versus Cav1-KO (open bars) CD8 T cells to ICAM-1. CD8 T cells were stimulated with 50 nM PdBu, 1 μg/ml anti-CD3 Ab, or 5 μg/ml SDF-1α before the start of the assay. Fluid shear flow rates were set at 0.3 dyne/cm 2 . ( B ) Rolling rates of the cells were analyzed in parallel with ( C ) the number of adherent cells. Data are shown as mean ± SEM of data pooled from two independent experiments, each performed in triplicate on two mice per group. * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001 (Student t test). ( D ) Cav1-WT or Cav1-KO OT-1 CD8 T cells were incubated for 30 min with chimeric ICAM-1 in HEPES buffer alone or supplemented with 100 nM Mg 2+ , or stimulated with PdBu, N4 peptide, anti-CD3, or anti-CD3 plus anti-CD28, as indicated. ICAM-1 bound to T cells was detected by staining with human IgG-FITC. ICAM-1 MFI ± SEM from one of three independent experiments. ( E ) Representative histograms from each condition, as indicated. ns, not significant.
Figure Legend Snippet: Impaired adhesion to ICAM-1 under conditions of fluid shear stress in the absence of Cav1. ( A ) Static adhesion of WT (filled bars) versus Cav1-KO (open bars) CD8 T cells to ICAM-1. CD8 T cells were stimulated with 50 nM PdBu, 1 μg/ml anti-CD3 Ab, or 5 μg/ml SDF-1α before the start of the assay. Fluid shear flow rates were set at 0.3 dyne/cm 2 . ( B ) Rolling rates of the cells were analyzed in parallel with ( C ) the number of adherent cells. Data are shown as mean ± SEM of data pooled from two independent experiments, each performed in triplicate on two mice per group. * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001 (Student t test). ( D ) Cav1-WT or Cav1-KO OT-1 CD8 T cells were incubated for 30 min with chimeric ICAM-1 in HEPES buffer alone or supplemented with 100 nM Mg 2+ , or stimulated with PdBu, N4 peptide, anti-CD3, or anti-CD3 plus anti-CD28, as indicated. ICAM-1 bound to T cells was detected by staining with human IgG-FITC. ICAM-1 MFI ± SEM from one of three independent experiments. ( E ) Representative histograms from each condition, as indicated. ns, not significant.

Techniques Used: Flow Cytometry, Mouse Assay, Incubation, Staining

Absence of Cav1 alters CD8 T cell morphology and polarization upon adhesion to ICAM-1. Cav1-WT and Cav1-KO OT-1 CD8 T cells were allowed to adhere for 30 min to glass slides with and without 3 μg/ml ICAM-1 coating. ( A ) Cells were stained with BODIPY-Fl (green) to define the cell perimeter. Cav1-WT and Cav1-KO CD8 T cells spreading on ICAM-1 were quantified in terms of ( B ) area, ( C ) longest axis, and ( D ) shape factor. For shape factor, a value of 1 is circular. (B–D) Small horizontal lines indicate the mean. ( E and F ) Cells were stained with Ezrin (green) and Lck (red). Merge images were sectioned (white line) from the leading edge, indicated by the asterisk, to the uropod, generating an RGB histogram using ImageJ software. The histogram line indicates the distribution and MFI of proteins throughout the cross-section of the cell. ( G ) A Pearson correlation coefficient was calculated by Volocity software, and p values were calculated by the Student t test. Data are representative of one of three independent experiments with a minimum of 100 cells per condition. Scale bars, 1 μm. **** p ≤ 0.001.
Figure Legend Snippet: Absence of Cav1 alters CD8 T cell morphology and polarization upon adhesion to ICAM-1. Cav1-WT and Cav1-KO OT-1 CD8 T cells were allowed to adhere for 30 min to glass slides with and without 3 μg/ml ICAM-1 coating. ( A ) Cells were stained with BODIPY-Fl (green) to define the cell perimeter. Cav1-WT and Cav1-KO CD8 T cells spreading on ICAM-1 were quantified in terms of ( B ) area, ( C ) longest axis, and ( D ) shape factor. For shape factor, a value of 1 is circular. (B–D) Small horizontal lines indicate the mean. ( E and F ) Cells were stained with Ezrin (green) and Lck (red). Merge images were sectioned (white line) from the leading edge, indicated by the asterisk, to the uropod, generating an RGB histogram using ImageJ software. The histogram line indicates the distribution and MFI of proteins throughout the cross-section of the cell. ( G ) A Pearson correlation coefficient was calculated by Volocity software, and p values were calculated by the Student t test. Data are representative of one of three independent experiments with a minimum of 100 cells per condition. Scale bars, 1 μm. **** p ≤ 0.001.

Techniques Used: Staining, Software

21) Product Images from "Altered Monocyte and Endothelial Cell Adhesion Molecule Expression Is Linked to Vascular Inflammation in Human Immunodeficiency Virus Infection"

Article Title: Altered Monocyte and Endothelial Cell Adhesion Molecule Expression Is Linked to Vascular Inflammation in Human Immunodeficiency Virus Infection

Journal: Open Forum Infectious Diseases

doi: 10.1093/ofid/ofw224

Plasma levels of inflammatory markers and endothelial adhesion molecules are elevated in human immunodeficiency virus (HIV)-infected participants. Plasma samples from all participants were thawed, and levels of soluble markers were measured using commercial enzyme-linked immunosorbent assays. Comparative data between HIV-positive (HIV + ) and HIV-negative (HIV − ) participants for inflammatory markers are shown as medians (with interquartile ranges) for levels of the following: (A) soluble (s)CD14, sCD163, tumor necrosis factor receptor (TNFR)-I, and TNFR-II; (B) vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, ICAM-2, and fractalkine; and (C) lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ). (D) The representative correlation graphs between inflammatory markers and endothelial adhesion molecules among samples from HIV + participants are shown. Levels of VCAM-1 (left) were associated with levels of sCD14, TNFR-I, TNFR-II, and ICAM-1. Levels of ICAM-1 (right) were associated with levels of sCD14, TNFR-I, TNFR-II, and fractalkine.
Figure Legend Snippet: Plasma levels of inflammatory markers and endothelial adhesion molecules are elevated in human immunodeficiency virus (HIV)-infected participants. Plasma samples from all participants were thawed, and levels of soluble markers were measured using commercial enzyme-linked immunosorbent assays. Comparative data between HIV-positive (HIV + ) and HIV-negative (HIV − ) participants for inflammatory markers are shown as medians (with interquartile ranges) for levels of the following: (A) soluble (s)CD14, sCD163, tumor necrosis factor receptor (TNFR)-I, and TNFR-II; (B) vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, ICAM-2, and fractalkine; and (C) lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ). (D) The representative correlation graphs between inflammatory markers and endothelial adhesion molecules among samples from HIV + participants are shown. Levels of VCAM-1 (left) were associated with levels of sCD14, TNFR-I, TNFR-II, and ICAM-1. Levels of ICAM-1 (right) were associated with levels of sCD14, TNFR-I, TNFR-II, and fractalkine.

Techniques Used: Infection, Proximity Ligation Assay

22) Product Images from "Lung-Targeted Overexpression of the NF-?B Member RelB Inhibits Cigarette Smoke-Induced Inflammation"

Article Title: Lung-Targeted Overexpression of the NF-?B Member RelB Inhibits Cigarette Smoke-Induced Inflammation

Journal: The American Journal of Pathology

doi: 10.1016/j.ajpath.2011.03.030

RelB overexpression reduces cigarette smoke–induced ICAM-1 expression in mouse lungs. Mice were treated with either the RelB or control virus (two doses of 5 × 10 8 plaque-forming units per mouse delivered 24 hours apart) and exposed to
Figure Legend Snippet: RelB overexpression reduces cigarette smoke–induced ICAM-1 expression in mouse lungs. Mice were treated with either the RelB or control virus (two doses of 5 × 10 8 plaque-forming units per mouse delivered 24 hours apart) and exposed to

Techniques Used: Over Expression, Expressing, Mouse Assay

23) Product Images from "Determining \u03b22-Integrin and Intercellular Adhesion Molecule 1 Binding Kinetics in Tumor Cell Adhesion to Leukocytes and Endothelial Cells by a Gas-driven Micropipette Assay"

Article Title: Determining \u03b22-Integrin and Intercellular Adhesion Molecule 1 Binding Kinetics in Tumor Cell Adhesion to Leukocytes and Endothelial Cells by a Gas-driven Micropipette Assay

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M111.281642

Expression of β 2 -integrin and ICAM-1 molecules on PMNs ( A ), WM9 cells ( B ), and HPMECs ( C ). The cells were incubated with the respective blocking mAbs followed by secondary FITC-conjugated mAbs ( unfilled histograms ), whereas the blank cells were
Figure Legend Snippet: Expression of β 2 -integrin and ICAM-1 molecules on PMNs ( A ), WM9 cells ( B ), and HPMECs ( C ). The cells were incubated with the respective blocking mAbs followed by secondary FITC-conjugated mAbs ( unfilled histograms ), whereas the blank cells were

Techniques Used: Expressing, Incubation, Blocking Assay

24) Product Images from "Endothelial microparticles interact with and support the proliferation of T cells"

Article Title: Endothelial microparticles interact with and support the proliferation of T cells

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1303431

EMP bind preferentially to memory T cells and TNF+IFNγ EMP bind to T cells in an ICAM-1/VCAM-1 dependent manner
Figure Legend Snippet: EMP bind preferentially to memory T cells and TNF+IFNγ EMP bind to T cells in an ICAM-1/VCAM-1 dependent manner

Techniques Used:

25) Product Images from "OxLDL and substrate stiffness promote neutrophil transmigration by enhanced endothelial cell contractility and ICAM-1"

Article Title: OxLDL and substrate stiffness promote neutrophil transmigration by enhanced endothelial cell contractility and ICAM-1

Journal: Journal of Biomechanics

doi: 10.1016/j.jbiomech.2012.04.011

ICAM-1 expression is enhanced in 24-hour oxLDL-treated HUVECs, and blocking ICAM-1 significantly reduces transmgiration on all substrates. (A) HUVECs were immunostained for ICAM-1 and fluorescence images were taken at many different locations across each of at least 3 different monolayers for each substrate. Bars are mean ± standard error of 3 experiments. P > 0.05 by ANOVA across substrates for untreated and oxLDL-treated HUVECs. For each substrate, * indicates that P
Figure Legend Snippet: ICAM-1 expression is enhanced in 24-hour oxLDL-treated HUVECs, and blocking ICAM-1 significantly reduces transmgiration on all substrates. (A) HUVECs were immunostained for ICAM-1 and fluorescence images were taken at many different locations across each of at least 3 different monolayers for each substrate. Bars are mean ± standard error of 3 experiments. P > 0.05 by ANOVA across substrates for untreated and oxLDL-treated HUVECs. For each substrate, * indicates that P

Techniques Used: Expressing, Blocking Assay, Fluorescence

26) Product Images from "Endothelial Activation and Cell Adhesion Molecule Concentrations in Pregnant Women Living at High Altitude"

Article Title: Endothelial Activation and Cell Adhesion Molecule Concentrations in Pregnant Women Living at High Altitude

Journal: Journal of the Society for Gynecologic Investigation

doi: 10.1016/j.jsgi.2006.05.001

ICAM-1 concentrations throughout pregnancy at moderate altitude ( open circles ) and high altitude ( shaded circles ).
Figure Legend Snippet: ICAM-1 concentrations throughout pregnancy at moderate altitude ( open circles ) and high altitude ( shaded circles ).

Techniques Used:

27) Product Images from "Differential Transmission of Human Immunodeficiency Virus Type 1 by Distinct Subsets of Effector Dendritic Cells"

Article Title: Differential Transmission of Human Immunodeficiency Virus Type 1 by Distinct Subsets of Effector Dendritic Cells

Journal: Journal of Virology

doi: 10.1128/JVI.76.15.7812-7821.2002

). (B) In HIV-1 transmission, DC-SIGN captures the virus particle through interaction with gp120 (14). When the DC subsequently contact T cells through the ICAM-1-LFA-1 interaction, HIV-1 is juxtaposed to the T-cell surface with the CD4 and CXCR4 receptors.
Figure Legend Snippet: ). (B) In HIV-1 transmission, DC-SIGN captures the virus particle through interaction with gp120 (14). When the DC subsequently contact T cells through the ICAM-1-LFA-1 interaction, HIV-1 is juxtaposed to the T-cell surface with the CD4 and CXCR4 receptors.

Techniques Used: Transmission Assay

Cell-cell contact via ICAM-1-LFA-1 is essential for DC1-mediated transmission. (A) Blocking of ICAM-1. Transmission of HIV-1 by DC was performed in the absence or presence of a neutralizing anti-ICAM-1 antibody. The antibody was present in the 2-h DC-HIV-1 incubation and washed out together with unbound virus prior to coculture with T cells. The DC1 cells used in this experiment were obtained by poly(I-C) stimulation. The right two bars represent a normal infection control. No wash was performed with these samples. (B) DC-mediated transmission was performed with or without a permeable membrane (transwell) between the virus-preincubated DC and T cells. (C) Effect of DC-conditioned medium on regular T-cell infection. SupT1 cells were infected with HIV-1 (150 pg of CA-p24) in the presence or absence of the respective DC supernatants. The CA-p24 values measured at day 3 postinfection are shown. (D) Virus capture by DC. DC (150 × 10 3 ) were incubated with virus (20 ng of CA-p24) for 2 h. After extensive washing, DC were lysed, and bound virus was quantitated by ELISA.
Figure Legend Snippet: Cell-cell contact via ICAM-1-LFA-1 is essential for DC1-mediated transmission. (A) Blocking of ICAM-1. Transmission of HIV-1 by DC was performed in the absence or presence of a neutralizing anti-ICAM-1 antibody. The antibody was present in the 2-h DC-HIV-1 incubation and washed out together with unbound virus prior to coculture with T cells. The DC1 cells used in this experiment were obtained by poly(I-C) stimulation. The right two bars represent a normal infection control. No wash was performed with these samples. (B) DC-mediated transmission was performed with or without a permeable membrane (transwell) between the virus-preincubated DC and T cells. (C) Effect of DC-conditioned medium on regular T-cell infection. SupT1 cells were infected with HIV-1 (150 pg of CA-p24) in the presence or absence of the respective DC supernatants. The CA-p24 values measured at day 3 postinfection are shown. (D) Virus capture by DC. DC (150 × 10 3 ) were incubated with virus (20 ng of CA-p24) for 2 h. After extensive washing, DC were lysed, and bound virus was quantitated by ELISA.

Techniques Used: Transmission Assay, Blocking Assay, Incubation, Infection, Enzyme-linked Immunosorbent Assay

28) Product Images from "Renal cell carcinoma alters endothelial receptor expression responsible for leukocyte adhesion"

Article Title: Renal cell carcinoma alters endothelial receptor expression responsible for leukocyte adhesion

Journal: Oncotarget

doi: 10.18632/oncotarget.7804

Impact of alteration in endothelial receptor expression on PBL and PMN adhesion to endothelium 12h stimulation with TNF-alpha [500 U/ml] and/or 1h functional blocking of endothelial ICAM-1, VCAM-1, E-selectin and CD44 by monoclonal antibodies. Unblocked HUVEC cells served as controls. Mean number of adherent PBLs and PMNs from five fields (0.25 mm 2 ) were evaluated and expressed as % of adherent control cells (100%). *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha stimulated HUVEC. n=5.
Figure Legend Snippet: Impact of alteration in endothelial receptor expression on PBL and PMN adhesion to endothelium 12h stimulation with TNF-alpha [500 U/ml] and/or 1h functional blocking of endothelial ICAM-1, VCAM-1, E-selectin and CD44 by monoclonal antibodies. Unblocked HUVEC cells served as controls. Mean number of adherent PBLs and PMNs from five fields (0.25 mm 2 ) were evaluated and expressed as % of adherent control cells (100%). *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha stimulated HUVEC. n=5.

Techniques Used: Expressing, Functional Assay, Blocking Assay

Endothelial surface expression of adhesion receptors on HMEC-1 and HC-6014 cells after TNF-alpha [500 U/ml] stimulation and/or co-cultivation with Caki-1 cells Expression of ICAM-1, VCAM-1 and E-selectin after 24h TNF-alpha [500 U/ml] stimulation. MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha stimulated HUVEC. n=5.
Figure Legend Snippet: Endothelial surface expression of adhesion receptors on HMEC-1 and HC-6014 cells after TNF-alpha [500 U/ml] stimulation and/or co-cultivation with Caki-1 cells Expression of ICAM-1, VCAM-1 and E-selectin after 24h TNF-alpha [500 U/ml] stimulation. MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha stimulated HUVEC. n=5.

Techniques Used: Expressing, Fluorescence

A. Western Blot Analysis. Total protein content of ICAM-1, VCAM-1 and E-selectin in HUVEC cells incubated with TNF-alpha (500 U/ml) and/or Caki-1 cell fragments for 24h. TNF = TNF-alpha, Caki-1 frag. = Caki-1 cell fragments. B. Pixel density of protein bands shown in A.
Figure Legend Snippet: A. Western Blot Analysis. Total protein content of ICAM-1, VCAM-1 and E-selectin in HUVEC cells incubated with TNF-alpha (500 U/ml) and/or Caki-1 cell fragments for 24h. TNF = TNF-alpha, Caki-1 frag. = Caki-1 cell fragments. B. Pixel density of protein bands shown in A.

Techniques Used: Western Blot, Incubation

Influence of supernatants (culture medium) from Caki-1 or Caki-1-HUVEC co-culture FACscan analysis of ICAM-1, VCAM-1, E-selectin, CD44 V3 and CD44 V7 after 12h TNF-alpha [500 U/ml] stimulation and/or co-cultivation with Caki-1 or co-culture supernatants (culture medium). MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha stimulated HUVEC. n=5.
Figure Legend Snippet: Influence of supernatants (culture medium) from Caki-1 or Caki-1-HUVEC co-culture FACscan analysis of ICAM-1, VCAM-1, E-selectin, CD44 V3 and CD44 V7 after 12h TNF-alpha [500 U/ml] stimulation and/or co-cultivation with Caki-1 or co-culture supernatants (culture medium). MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha stimulated HUVEC. n=5.

Techniques Used: Co-Culture Assay, Fluorescence

A. Magnet bead separation of Caki-1 and HUVEC from the co-culture by epithelial CD326. Black line: isotype control, green line: unstimulated cells, red line: TNF-alpha (24h, 500 U/ml) stimulated cells. One representative of three separate experiments is shown. B. Western Blot Analysis. Total protein content of ICAM-1, VCAM-1, E-selectin and CD144 (endothelial control) in Caki-1 and HUVEC cells separated by magnet beads. HUVEC + Caki = HUVEC separated from Caki-1 co-culture. Caki-1 and HUVEC cells, cultivated separately, served as controls. n.d. = not detectable. C. Pixel density of protein bands shown in B.
Figure Legend Snippet: A. Magnet bead separation of Caki-1 and HUVEC from the co-culture by epithelial CD326. Black line: isotype control, green line: unstimulated cells, red line: TNF-alpha (24h, 500 U/ml) stimulated cells. One representative of three separate experiments is shown. B. Western Blot Analysis. Total protein content of ICAM-1, VCAM-1, E-selectin and CD144 (endothelial control) in Caki-1 and HUVEC cells separated by magnet beads. HUVEC + Caki = HUVEC separated from Caki-1 co-culture. Caki-1 and HUVEC cells, cultivated separately, served as controls. n.d. = not detectable. C. Pixel density of protein bands shown in B.

Techniques Used: Co-Culture Assay, Western Blot

Impact of Caki-1 cell fragments on endothelial surface expression FACscan analysis of ICAM-1, VCAM-1, E-selectin, CD44 V3 and CD44 V7 after 12h TNF-alpha [500 U/ml] stimulation and/or co-cultivation with Caki-1 cell fragments. MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha stimulated HUVEC. n=5.
Figure Legend Snippet: Impact of Caki-1 cell fragments on endothelial surface expression FACscan analysis of ICAM-1, VCAM-1, E-selectin, CD44 V3 and CD44 V7 after 12h TNF-alpha [500 U/ml] stimulation and/or co-cultivation with Caki-1 cell fragments. MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha stimulated HUVEC. n=5.

Techniques Used: Expressing, Fluorescence

Endothelial surface expression of adhesion receptors in HUVEC after cytokine stimulation and/or co-cultivation with Caki-1 cells Expression of ICAM-1, VCAM-1 and E-selectin after 24h TNF-alpha [500 U/ml] and P-selectin after 10 min histamine [100 μM/ml] stimulation. MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha/histamine stimulated HUVEC. n=5.
Figure Legend Snippet: Endothelial surface expression of adhesion receptors in HUVEC after cytokine stimulation and/or co-cultivation with Caki-1 cells Expression of ICAM-1, VCAM-1 and E-selectin after 24h TNF-alpha [500 U/ml] and P-selectin after 10 min histamine [100 μM/ml] stimulation. MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha/histamine stimulated HUVEC. n=5.

Techniques Used: Expressing, Fluorescence

Endothelial surface expression of adhesion receptors on HUVEC after TNF-alpha [500 U/ml] stimulation and/or co-cultivation with Caki-1 cells under flow conditions Expression of ICAM-1, VCAM-1 and E-selectin after 24h TNF-alpha [500 U/ml] stimulation. MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha/histamine stimulated HUVEC. n=6.
Figure Legend Snippet: Endothelial surface expression of adhesion receptors on HUVEC after TNF-alpha [500 U/ml] stimulation and/or co-cultivation with Caki-1 cells under flow conditions Expression of ICAM-1, VCAM-1 and E-selectin after 24h TNF-alpha [500 U/ml] stimulation. MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha/histamine stimulated HUVEC. n=6.

Techniques Used: Expressing, Flow Cytometry, Fluorescence

HUVEC conditioning of surface expression by Caki-1 membrane proteins FACscan analysis of ICAM-1, VCAM-1, E-selectin, CD44 V3 and CD44 V7 after 12h TNF alpha [500 U/ml] stimulation and/or co-cultivation with Caki-1 membrane proteins. MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha stimulated HUVEC. n=5.
Figure Legend Snippet: HUVEC conditioning of surface expression by Caki-1 membrane proteins FACscan analysis of ICAM-1, VCAM-1, E-selectin, CD44 V3 and CD44 V7 after 12h TNF alpha [500 U/ml] stimulation and/or co-cultivation with Caki-1 membrane proteins. MFI = mean relative fluorescence intensity. *indicates significant difference to untreated controls. #indicates significant difference to TNF-alpha stimulated HUVEC. n=5.

Techniques Used: Expressing, Fluorescence

29) Product Images from "Sensitive Plasma Protein Analysis by Microparticle-based Proximity Ligation Assays *"

Article Title: Sensitive Plasma Protein Analysis by Microparticle-based Proximity Ligation Assays *

Journal: Molecular & Cellular Proteomics : MCP

doi: 10.1074/mcp.M900248-MCP200

Detection of ICAM-1, GDF-15, TNFα, IL-4, PSA, and p53 with SP-PLA in 10% serum ( triangles ) and 10% plasma ( diamonds ). y axes display threshold cycle values of real time PCR assays; x axes display concentration of each antigen in p m .
Figure Legend Snippet: Detection of ICAM-1, GDF-15, TNFα, IL-4, PSA, and p53 with SP-PLA in 10% serum ( triangles ) and 10% plasma ( diamonds ). y axes display threshold cycle values of real time PCR assays; x axes display concentration of each antigen in p m .

Techniques Used: Proximity Ligation Assay, Real-time Polymerase Chain Reaction, Concentration Assay

30) Product Images from "Quercetin inhibits LPS-induced adhesion molecule expression and oxidant production in human aortic endothelial cells by p38-mediated Nrf2 activation and antioxidant enzyme induction"

Article Title: Quercetin inhibits LPS-induced adhesion molecule expression and oxidant production in human aortic endothelial cells by p38-mediated Nrf2 activation and antioxidant enzyme induction

Journal: Redox Biology

doi: 10.1016/j.redox.2016.06.006

Quercetin inhibits LPS-induced adhesion molecule expression. Human aortic endothelial cells were incubated for 18 h without or with the indicated concentrations of quercetin, and then were co-incubated for 3 h (mRNA levels) or 5 h (protein levels) without or with 0.10 µg/ml LPS and the corresponding concentrations of quercetin. mRNA and protein levels of E-selectin (a, c) and ICAM-1 (b, d) were measured by real-time PCR and cell-ELISA, respectively. *Denotes significant difference from LPS-stimulated cells, P
Figure Legend Snippet: Quercetin inhibits LPS-induced adhesion molecule expression. Human aortic endothelial cells were incubated for 18 h without or with the indicated concentrations of quercetin, and then were co-incubated for 3 h (mRNA levels) or 5 h (protein levels) without or with 0.10 µg/ml LPS and the corresponding concentrations of quercetin. mRNA and protein levels of E-selectin (a, c) and ICAM-1 (b, d) were measured by real-time PCR and cell-ELISA, respectively. *Denotes significant difference from LPS-stimulated cells, P

Techniques Used: Expressing, Incubation, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

31) Product Images from "The association between metabolic components and markers of inflammatory and endothelial dysfunction in adolescents, based on the Ewha Birth and Growth Cohort Study"

Article Title: The association between metabolic components and markers of inflammatory and endothelial dysfunction in adolescents, based on the Ewha Birth and Growth Cohort Study

Journal: PLoS ONE

doi: 10.1371/journal.pone.0233469

Effects of metabolic factors on the association between BMI and elevated levels of hs-CRP (A), ICAM-1 (B), and VCAM-1 (C). Abbreviation : BMI, body mass index; MAP, mean arterial pressure; TG, triglyceride; HDL-c, high-density lipoprotein cholesterol; hs-CRP, high-sensitivity C-reactive protein; ICAM-1, intercellular adhesion molecule; VCAM-1, vascular cell adhesion molecule. a p
Figure Legend Snippet: Effects of metabolic factors on the association between BMI and elevated levels of hs-CRP (A), ICAM-1 (B), and VCAM-1 (C). Abbreviation : BMI, body mass index; MAP, mean arterial pressure; TG, triglyceride; HDL-c, high-density lipoprotein cholesterol; hs-CRP, high-sensitivity C-reactive protein; ICAM-1, intercellular adhesion molecule; VCAM-1, vascular cell adhesion molecule. a p

Techniques Used:

32) Product Images from "Blockade of vascular adhesion protein-1 attenuates choroidal neovascularization"

Article Title: Blockade of vascular adhesion protein-1 attenuates choroidal neovascularization

Journal: Molecular Vision

doi:

Impact of VAP-1 blockade on inflammation-associated molecules. Bars indicate the average protein levels of ( A ) ICAM-1, ( B ) MCP-1, (C) P-selectin, and ( D ) VEGF in the RPE-choroidal complex obtained from laser-induced CNV animals treated with vehicle or VAP-1 inhibitor at 3 days after laser photocoagulation. Values are mean±SEM (n=9 to 10). *, p
Figure Legend Snippet: Impact of VAP-1 blockade on inflammation-associated molecules. Bars indicate the average protein levels of ( A ) ICAM-1, ( B ) MCP-1, (C) P-selectin, and ( D ) VEGF in the RPE-choroidal complex obtained from laser-induced CNV animals treated with vehicle or VAP-1 inhibitor at 3 days after laser photocoagulation. Values are mean±SEM (n=9 to 10). *, p

Techniques Used:

33) Product Images from "The presence of alpha-catenin in the VE-cadherin complex is required for efficient transendothelial migration of leukocytes"

Article Title: The presence of alpha-catenin in the VE-cadherin complex is required for efficient transendothelial migration of leukocytes

Journal: International Journal of Biological Sciences

doi:

Effects of S27D on viability on endothelial cells. ( A ) TNF-α-stimulated HUVEC were treated for 30 minutes with S27D (5μg/mL), control peptide (CTRL) or DMSO and subsequently trypsinized, fixed and stained with Annexin-V-FITC and Propidium iodide (PI). Plots show that after S27D treatment, 77% of the cells were negative for Annexin-V. After DMSO and control peptide (CTRL) treatment, respectively 89% and 88% of the cells were negative. All cells were negative for PI, showing that the treatment did not induce necrosis. Neutrophils (PMN) were left overnight (O/N) and used as positive Annexin-V control. Only 15% of the PMNs were Annexin-V negative. ( B ) Effect of S27D on apoptosis of endothelial cells at different time points are analyzed using Annexin-V-FITC labeling. Experiment is carried out three times. Data are mean ± SEM. ( C ) HUVEC were treated as described under A. Expression of ICAM-1, VCAM-1, PECAM-1 and VE-cadherin was measured by flow cytometry analysis and expressed as Mean fluorescent Intensity (MFI) arbitrary units on the Y-axis. S27D was incubated for different time points as indicated. VE-cadherin expression is increased after overnight treatment with S27D. Experiment was carried out three times in triplicate. Data are mean ± SEM. *p
Figure Legend Snippet: Effects of S27D on viability on endothelial cells. ( A ) TNF-α-stimulated HUVEC were treated for 30 minutes with S27D (5μg/mL), control peptide (CTRL) or DMSO and subsequently trypsinized, fixed and stained with Annexin-V-FITC and Propidium iodide (PI). Plots show that after S27D treatment, 77% of the cells were negative for Annexin-V. After DMSO and control peptide (CTRL) treatment, respectively 89% and 88% of the cells were negative. All cells were negative for PI, showing that the treatment did not induce necrosis. Neutrophils (PMN) were left overnight (O/N) and used as positive Annexin-V control. Only 15% of the PMNs were Annexin-V negative. ( B ) Effect of S27D on apoptosis of endothelial cells at different time points are analyzed using Annexin-V-FITC labeling. Experiment is carried out three times. Data are mean ± SEM. ( C ) HUVEC were treated as described under A. Expression of ICAM-1, VCAM-1, PECAM-1 and VE-cadherin was measured by flow cytometry analysis and expressed as Mean fluorescent Intensity (MFI) arbitrary units on the Y-axis. S27D was incubated for different time points as indicated. VE-cadherin expression is increased after overnight treatment with S27D. Experiment was carried out three times in triplicate. Data are mean ± SEM. *p

Techniques Used: Staining, Labeling, Expressing, Flow Cytometry, Cytometry, Incubation

34) Product Images from "Liver Restores Immune Homeostasis after Local Inflammation despite the Presence of Autoreactive T Cells"

Article Title: Liver Restores Immune Homeostasis after Local Inflammation despite the Presence of Autoreactive T Cells

Journal: PLoS ONE

doi: 10.1371/journal.pone.0048192

Adhesion Molecules VCAM-1 and ICAM-1, but not Vap-1, are Up-regulated in Response to Autoreactive Cells and TLRs Stimulation. Levels of specific mRNAs ( A, D, G ) and proteins expression ( B, E, H ) in the liver were measured for VCAM-1 ( A–C ), ICAM-1 ( D–F ) and Vap-1 ( G–I ). Only VCAM-1 mRNA was up-regulated in response to TLRs stimulation (ANOVA, p
Figure Legend Snippet: Adhesion Molecules VCAM-1 and ICAM-1, but not Vap-1, are Up-regulated in Response to Autoreactive Cells and TLRs Stimulation. Levels of specific mRNAs ( A, D, G ) and proteins expression ( B, E, H ) in the liver were measured for VCAM-1 ( A–C ), ICAM-1 ( D–F ) and Vap-1 ( G–I ). Only VCAM-1 mRNA was up-regulated in response to TLRs stimulation (ANOVA, p

Techniques Used: Expressing

35) Product Images from "TNF-α augmented Porphyromonas gingivalis invasion in human gingival epithelial cells through Rab5 and ICAM-1"

Article Title: TNF-α augmented Porphyromonas gingivalis invasion in human gingival epithelial cells through Rab5 and ICAM-1

Journal: BMC Microbiology

doi: 10.1186/s12866-014-0229-z

TNF-α increased colocalization of P. gingivalis with ICAM-1 and Rab5. Ca9-22 cells were transfected with expression vectors with inserted genes of GFP-Rab5. The cells were treated with TNF-α for 3 h and were further incubated with P. gingivalis for 1 h. The cells were then stained using an anti-ICAM-1 antibody and anti- P. gingivalis antisera. Each molecule was visualized as follows: GFP-Rab5 (green), ICAM-1 (red), and P. gingivalis (blue).
Figure Legend Snippet: TNF-α increased colocalization of P. gingivalis with ICAM-1 and Rab5. Ca9-22 cells were transfected with expression vectors with inserted genes of GFP-Rab5. The cells were treated with TNF-α for 3 h and were further incubated with P. gingivalis for 1 h. The cells were then stained using an anti-ICAM-1 antibody and anti- P. gingivalis antisera. Each molecule was visualized as follows: GFP-Rab5 (green), ICAM-1 (red), and P. gingivalis (blue).

Techniques Used: Transfection, Expressing, Incubation, Staining

ICAM-1 mediates invasion of P. gingivalis. (A) Ca9-22 cells were incubated with P. gingivalis for 1 h. The cells were then stained using anti-ICAM-1 antibody. ICAM-1 is shown in green and P. gingivalis is shown in red. Bars in each panel are 10 μm. (B) TNF-α increased expression of ICAM-1 in Ca9-22 cells. Ca9-22 cells were treated with 10 ng/ml of TNF-α for 3 h. The cells were lysed and the expression of ICAM-1 and Rab5 was analyzed by Western blotting with antibodies for each molecule. (C) Antibody to ICAM-1 inhibits invasion of P. gingivalis in cells. Ca9-22 cells were treated with TNF-α for 3 h and were then incubated with an anti-ICAM-1 antibody or a control IgG antibody for 2 h. Viable P. gingivalis in the cells was determined as described in Methods . (Means ± standard deviations [SD] [n = 3]). ††, P
Figure Legend Snippet: ICAM-1 mediates invasion of P. gingivalis. (A) Ca9-22 cells were incubated with P. gingivalis for 1 h. The cells were then stained using anti-ICAM-1 antibody. ICAM-1 is shown in green and P. gingivalis is shown in red. Bars in each panel are 10 μm. (B) TNF-α increased expression of ICAM-1 in Ca9-22 cells. Ca9-22 cells were treated with 10 ng/ml of TNF-α for 3 h. The cells were lysed and the expression of ICAM-1 and Rab5 was analyzed by Western blotting with antibodies for each molecule. (C) Antibody to ICAM-1 inhibits invasion of P. gingivalis in cells. Ca9-22 cells were treated with TNF-α for 3 h and were then incubated with an anti-ICAM-1 antibody or a control IgG antibody for 2 h. Viable P. gingivalis in the cells was determined as described in Methods . (Means ± standard deviations [SD] [n = 3]). ††, P

Techniques Used: Incubation, Staining, Expressing, Western Blot

36) Product Images from "ASIC1a induces synovial inflammation via the Ca2+/NFATc3/ RANTES pathway"

Article Title: ASIC1a induces synovial inflammation via the Ca2+/NFATc3/ RANTES pathway

Journal: Theranostics

doi: 10.7150/thno.37200

ASIC1a upregulates the expression of inflammatory cytokines by mediating Ca 2+ influx. (A) 40 inflammatory cytokines were analyzed by KEGG pathway enrichment analysis. (B) An inflammatory cytokines antibody array was used to examine the expression of 40 inflammatory cytokines in RASF with 100 nM PcTx-1. (C) Semi-quantitative analysis of the expressions of RANTES, sTNF RI, MIP-1a, IL-8, sTNF RII, and ICAM-1 by fluorescence intensity presented by heat map. (D) RANTES, sTNF RI, MIP-1a, IL-8, sTNF RII, and ICAM-1 were analyzed by KEGG pathway enrichment analysis. (E) The expression of RANTES was determined by magnetic multi-cytokine assay. Cells were treated for 6 h with100 nM PcTx-1. (F) Magnetic multi-cytokine assay detected the increase of RANTES expression mediated by ASIC1a in RASF treated for 6 h with 1 mM EGTA, 10 μM BAPTA-AM, 5 μM verapamil and HMA. Student´s t-test or one-way ANOVA was used for statistical analysis, and data are expressed as mean ± SEM for three separate experiments.
Figure Legend Snippet: ASIC1a upregulates the expression of inflammatory cytokines by mediating Ca 2+ influx. (A) 40 inflammatory cytokines were analyzed by KEGG pathway enrichment analysis. (B) An inflammatory cytokines antibody array was used to examine the expression of 40 inflammatory cytokines in RASF with 100 nM PcTx-1. (C) Semi-quantitative analysis of the expressions of RANTES, sTNF RI, MIP-1a, IL-8, sTNF RII, and ICAM-1 by fluorescence intensity presented by heat map. (D) RANTES, sTNF RI, MIP-1a, IL-8, sTNF RII, and ICAM-1 were analyzed by KEGG pathway enrichment analysis. (E) The expression of RANTES was determined by magnetic multi-cytokine assay. Cells were treated for 6 h with100 nM PcTx-1. (F) Magnetic multi-cytokine assay detected the increase of RANTES expression mediated by ASIC1a in RASF treated for 6 h with 1 mM EGTA, 10 μM BAPTA-AM, 5 μM verapamil and HMA. Student´s t-test or one-way ANOVA was used for statistical analysis, and data are expressed as mean ± SEM for three separate experiments.

Techniques Used: Expressing, Ab Array, Fluorescence, Cytokine Assay

37) Product Images from "Midkine drives cardiac inflammation by promoting neutrophil trafficking and NETosis in myocarditis"

Article Title: Midkine drives cardiac inflammation by promoting neutrophil trafficking and NETosis in myocarditis

Journal: The Journal of Experimental Medicine

doi: 10.1084/jem.20181102

LRP1-mediated PMN recruitment is MK dependent. (a) Representative images of dHoxb8- LRP1 ctrl cells on microflow chambers coated with recombinant P-selectin, ICAM-1, and MK. Cells were perfused through chambers with a shear rate of 1 dyne/cm 2 . Staining of cells was conducted using specific anti-LRP1 and anti-CD11a Abs, and imaging was performed using STED nanoscopy. Images show expression of LRP1 (green), CD11a (red), merge (yellow), and colocalization (coloc; pseudocolors [heat map]) of LRP1 and CD11a. The top panel illustrates an adherent cell and the lower panel a migrating cell. (b) Induction of adhesion of dHoxb8- LRP1 ctrl and dHoxb8- LRP1 cKO cells under flow conditions (1 dyne/cm 2 ) in microflow chambers coated with immobilized P-selectin, ICAM-1, and CXCL1 (dHoxb8- LRP1 ctrl , 100.0 [%]; dHoxb8- LRP1 cKO , 95.1 ± 12.7 [%]) or MK (dHoxb8- LRP1 ctrl , 100.0 [%]; dHoxb8- LRP1 cKO , 40.8 ± 6.0 [%]) as indicated. n = 4. (c and d) Migration of dHoxb8 cells under flow conditions. Euclidean distance (c; CXCL1: dHoxb8- LRP1 ctrl , 11.4 ± 2.2 µm; dHoxb8- LRP1 cKO , 9.4 ± 1.6 µm; MK: dHoxb8- LRP1 ctrl , 11.6 ± 0.55 µm; dHoxb8- LRP1 cKO , 6.56 ± 0.65 µm) as well as migration velocity (d; CXCL1: dHoxb8- LRP1 ctrl , 2.47 ± 0.25 µm/min; dHoxb8- LRP1 cKO , 2.41 ± 0.26 µm/min; MK: dHoxb8- LRP1 ctrl , 2.56 ± 0.16 µm/min; dHoxb8- LRP1 cKO , 1.54 ± 0.08 µm/min) of dHoxb8- LRP1 ctrl (white bar) and dHoxb8- LRP1 cKO (black bar) under flow conditions (1 dyne/cm 2 ). Flow chambers were coated with P-selectin, ICAM-1, and CXCL1 or MK as indicated. dHoxb8- LRP1 ctrl cells on CXCL1: n = 3 experiments/214 cells; dHoxb8- LRP1 cKO cells on CXCL1: n = 3 experiments/303 cells. dHoxb8- LRP1 ctrl cells on MK: n = 4 experiments/280 cells; dHoxb8- LRP1 cKO cells on MK: n = 4 experiments/197 cells. (e) Induction of adhesion of dHoxb8- LRP1 -NPxY ctrl and dHoxb8- LRP1 -NPxY ki cells under flow conditions (1 dyne/cm 2 ) in microflow chambers coated with immobilized P-selectin, ICAM-1, and CXCL1 (top diagram; dHoxb8- LRP1 -NPxY ctrl , 929.9 ± 62.9 cells; dHoxb8- LRP1 -NPxY ki , 762.8 ± 83.7 cells) or MK (bottom diagram; dHoxb8- LRP1 -NPxY ctrl , 953.3 ± 74.2 cells; dHoxb8- LRP1 -NPxY ki , 647.3 ± 101.8 cells). n = 6. To determine P values, an unpaired Student's t test was performed. For all panels, *, P
Figure Legend Snippet: LRP1-mediated PMN recruitment is MK dependent. (a) Representative images of dHoxb8- LRP1 ctrl cells on microflow chambers coated with recombinant P-selectin, ICAM-1, and MK. Cells were perfused through chambers with a shear rate of 1 dyne/cm 2 . Staining of cells was conducted using specific anti-LRP1 and anti-CD11a Abs, and imaging was performed using STED nanoscopy. Images show expression of LRP1 (green), CD11a (red), merge (yellow), and colocalization (coloc; pseudocolors [heat map]) of LRP1 and CD11a. The top panel illustrates an adherent cell and the lower panel a migrating cell. (b) Induction of adhesion of dHoxb8- LRP1 ctrl and dHoxb8- LRP1 cKO cells under flow conditions (1 dyne/cm 2 ) in microflow chambers coated with immobilized P-selectin, ICAM-1, and CXCL1 (dHoxb8- LRP1 ctrl , 100.0 [%]; dHoxb8- LRP1 cKO , 95.1 ± 12.7 [%]) or MK (dHoxb8- LRP1 ctrl , 100.0 [%]; dHoxb8- LRP1 cKO , 40.8 ± 6.0 [%]) as indicated. n = 4. (c and d) Migration of dHoxb8 cells under flow conditions. Euclidean distance (c; CXCL1: dHoxb8- LRP1 ctrl , 11.4 ± 2.2 µm; dHoxb8- LRP1 cKO , 9.4 ± 1.6 µm; MK: dHoxb8- LRP1 ctrl , 11.6 ± 0.55 µm; dHoxb8- LRP1 cKO , 6.56 ± 0.65 µm) as well as migration velocity (d; CXCL1: dHoxb8- LRP1 ctrl , 2.47 ± 0.25 µm/min; dHoxb8- LRP1 cKO , 2.41 ± 0.26 µm/min; MK: dHoxb8- LRP1 ctrl , 2.56 ± 0.16 µm/min; dHoxb8- LRP1 cKO , 1.54 ± 0.08 µm/min) of dHoxb8- LRP1 ctrl (white bar) and dHoxb8- LRP1 cKO (black bar) under flow conditions (1 dyne/cm 2 ). Flow chambers were coated with P-selectin, ICAM-1, and CXCL1 or MK as indicated. dHoxb8- LRP1 ctrl cells on CXCL1: n = 3 experiments/214 cells; dHoxb8- LRP1 cKO cells on CXCL1: n = 3 experiments/303 cells. dHoxb8- LRP1 ctrl cells on MK: n = 4 experiments/280 cells; dHoxb8- LRP1 cKO cells on MK: n = 4 experiments/197 cells. (e) Induction of adhesion of dHoxb8- LRP1 -NPxY ctrl and dHoxb8- LRP1 -NPxY ki cells under flow conditions (1 dyne/cm 2 ) in microflow chambers coated with immobilized P-selectin, ICAM-1, and CXCL1 (top diagram; dHoxb8- LRP1 -NPxY ctrl , 929.9 ± 62.9 cells; dHoxb8- LRP1 -NPxY ki , 762.8 ± 83.7 cells) or MK (bottom diagram; dHoxb8- LRP1 -NPxY ctrl , 953.3 ± 74.2 cells; dHoxb8- LRP1 -NPxY ki , 647.3 ± 101.8 cells). n = 6. To determine P values, an unpaired Student's t test was performed. For all panels, *, P

Techniques Used: Recombinant, Staining, Imaging, Expressing, Flow Cytometry, Migration

The MK receptor LRP1 is critical for leukocyte recruitment . (a–d) Intravital microscopy of cremaster muscle postcapillary venules of LRP1 ctrl and LRP1 cKO mice 2 h after intrascrotal application of TNFα. n = 18 venules from four LRP1 ctrl mice, n = 14 venules from three LRP1 cKO mice. (a) Leukocyte rolling flux fraction ( LRP1 ctrl , 0.097 ± 0.020 [%]; LRP1 cKO , 0.104 ± 0.032 [%]). (b) Leukocyte rolling velocity including 79 cells from four LRP1 ctrl mice and 71 cells from three LRP1 cKO mice ( LRP1 ctrl , 6.74 ± 0.24 µm/s; LRP1 cKO , 6.66 ± 0.17 µm/s). (c) Number of adherent leukocytes per mm 2 ( LRP1 ctrl , 1122.2 ± 133.2 cells/mm 2 ; LRP1 cKO , 456.0 ± 60.6 cells/mm 2 ). (d) Hemodynamic parameters of investigated vessels. (e) Differential cell counts of perivascular leukocytes as analyzed histologically in cremaster muscle whole mounts after Giemsa staining 2 h after intrascrotal application of TNFα. Eos, eosinophils; Others, lymphocytes, basophils and monocytes; n = 47 venules from four LRP1 ctrl mice, n = 28 from three LRP1 cKO mice (PMN: LRP1 ctrl , 958.3 ± 75.2 cells/mm 2 , LRP1 cKO , 354.1 ± 65 cells/mm 2 ). (f–h) Flow chamber assays with mPMN using spinning disk confocal microscopy after coating with P-selectin, ICAM-1, and CXCL1. (f) The intensity of LRP1 and CD11a as well as LRP1 and Gr-1 expression together with the merged (merge) or colocalized (coloc) intensity of one single representative cell is depicted during rolling and adhesion. Arrows indicate direction of flow. Right panels demonstrate the intensity of LRP1 and CD11a cell surface expression using pseudocolors (heat map). (g) Analysis of the intensity per area of colocalization of LRP1 or CD11a as well as of LRP1 or Gr-1, kinetics of rolling velocity and correlation of colocalization during rolling and adhesion of one representative cell. (h) Mean intensity per area of colocalization of LRP1 and CD11a (rolling, 0.071 ± 0.009 arbitrary units [a.u.]; adhesion, 0.255 ± 0.033 a.u.) as well as of LRP1 and Gr-1 (rolling, 0.280 ± 0.042 a.u.; adhesion, 0.299 ± 0.037 a.u.) during rolling and adhesion. LRP1/CD11a: n = 23 cells/five experiments, LRP1/Gr-1: n = 11 cells/three experiments. To determine P values, an unpaired Student's t test was performed for a–c and h, and ANOVA on ranks with Dunn’s multiple comparisons test was used for e. For all panels, *, P
Figure Legend Snippet: The MK receptor LRP1 is critical for leukocyte recruitment . (a–d) Intravital microscopy of cremaster muscle postcapillary venules of LRP1 ctrl and LRP1 cKO mice 2 h after intrascrotal application of TNFα. n = 18 venules from four LRP1 ctrl mice, n = 14 venules from three LRP1 cKO mice. (a) Leukocyte rolling flux fraction ( LRP1 ctrl , 0.097 ± 0.020 [%]; LRP1 cKO , 0.104 ± 0.032 [%]). (b) Leukocyte rolling velocity including 79 cells from four LRP1 ctrl mice and 71 cells from three LRP1 cKO mice ( LRP1 ctrl , 6.74 ± 0.24 µm/s; LRP1 cKO , 6.66 ± 0.17 µm/s). (c) Number of adherent leukocytes per mm 2 ( LRP1 ctrl , 1122.2 ± 133.2 cells/mm 2 ; LRP1 cKO , 456.0 ± 60.6 cells/mm 2 ). (d) Hemodynamic parameters of investigated vessels. (e) Differential cell counts of perivascular leukocytes as analyzed histologically in cremaster muscle whole mounts after Giemsa staining 2 h after intrascrotal application of TNFα. Eos, eosinophils; Others, lymphocytes, basophils and monocytes; n = 47 venules from four LRP1 ctrl mice, n = 28 from three LRP1 cKO mice (PMN: LRP1 ctrl , 958.3 ± 75.2 cells/mm 2 , LRP1 cKO , 354.1 ± 65 cells/mm 2 ). (f–h) Flow chamber assays with mPMN using spinning disk confocal microscopy after coating with P-selectin, ICAM-1, and CXCL1. (f) The intensity of LRP1 and CD11a as well as LRP1 and Gr-1 expression together with the merged (merge) or colocalized (coloc) intensity of one single representative cell is depicted during rolling and adhesion. Arrows indicate direction of flow. Right panels demonstrate the intensity of LRP1 and CD11a cell surface expression using pseudocolors (heat map). (g) Analysis of the intensity per area of colocalization of LRP1 or CD11a as well as of LRP1 or Gr-1, kinetics of rolling velocity and correlation of colocalization during rolling and adhesion of one representative cell. (h) Mean intensity per area of colocalization of LRP1 and CD11a (rolling, 0.071 ± 0.009 arbitrary units [a.u.]; adhesion, 0.255 ± 0.033 a.u.) as well as of LRP1 and Gr-1 (rolling, 0.280 ± 0.042 a.u.; adhesion, 0.299 ± 0.037 a.u.) during rolling and adhesion. LRP1/CD11a: n = 23 cells/five experiments, LRP1/Gr-1: n = 11 cells/three experiments. To determine P values, an unpaired Student's t test was performed for a–c and h, and ANOVA on ranks with Dunn’s multiple comparisons test was used for e. For all panels, *, P

Techniques Used: Intravital Microscopy, Mouse Assay, Staining, Flow Cytometry, Confocal Microscopy, Expressing

38) Product Images from "Danhong Huayu Koufuye Prevents Diabetic Retinopathy in Streptozotocin-Induced Diabetic Rats via Antioxidation and Anti-Inflammation"

Article Title: Danhong Huayu Koufuye Prevents Diabetic Retinopathy in Streptozotocin-Induced Diabetic Rats via Antioxidation and Anti-Inflammation

Journal: Mediators of Inflammation

doi: 10.1155/2017/3059763

Effects of DHK on serum levels of VEGF (a) and ICAM-1 (b) in rats. Seven days after injection of STZ, rats were orally administered for 16 weeks. At the end of the experiment, rats were anesthetized. Blood samples were collected to obtain serum. Levels of VEGF and ICAM-1 were measured with commercial assay kits. Values were expressed as mean ± SEM, n = 8–10, ∗ P
Figure Legend Snippet: Effects of DHK on serum levels of VEGF (a) and ICAM-1 (b) in rats. Seven days after injection of STZ, rats were orally administered for 16 weeks. At the end of the experiment, rats were anesthetized. Blood samples were collected to obtain serum. Levels of VEGF and ICAM-1 were measured with commercial assay kits. Values were expressed as mean ± SEM, n = 8–10, ∗ P

Techniques Used: Injection

Effect of DHK on mRNA expression of ICAM-1 in the retinas. Seven days after injection of STZ, rats were orally administered for 16 weeks. At the end of the experiment, rats were sacrificed and the left retinas were then collected. Retinal total RNA was extracted from the retina using TRIzol reagent. Retinal mRNA expression of ICAM-1 was evaluated using real-time PCR method. Results were expressed as percentage relative to the normal group. Values were expressed as mean ± SEM, n = 8–10, and ∗∗ P
Figure Legend Snippet: Effect of DHK on mRNA expression of ICAM-1 in the retinas. Seven days after injection of STZ, rats were orally administered for 16 weeks. At the end of the experiment, rats were sacrificed and the left retinas were then collected. Retinal total RNA was extracted from the retina using TRIzol reagent. Retinal mRNA expression of ICAM-1 was evaluated using real-time PCR method. Results were expressed as percentage relative to the normal group. Values were expressed as mean ± SEM, n = 8–10, and ∗∗ P

Techniques Used: Expressing, Injection, Real-time Polymerase Chain Reaction

39) Product Images from "Hepatoprotective Effects of Corilagin Following Hemorrhagic Shock are Through Akt-Dependent Pathway"

Article Title: Hepatoprotective Effects of Corilagin Following Hemorrhagic Shock are Through Akt-Dependent Pathway

Journal: Shock (Augusta, Ga.)

doi: 10.1097/SHK.0000000000000736

ICAM-1 levels in the liver in rats after sham operation (Sham) or hemorrhagic shock (H-S).
Figure Legend Snippet: ICAM-1 levels in the liver in rats after sham operation (Sham) or hemorrhagic shock (H-S).

Techniques Used:

40) Product Images from "cfDNA correlates with endothelial damage after cardiac surgery with prolonged cardiopulmonary bypass and amplifies NETosis in an intracellular TLR9-independent manner"

Article Title: cfDNA correlates with endothelial damage after cardiac surgery with prolonged cardiopulmonary bypass and amplifies NETosis in an intracellular TLR9-independent manner

Journal: Scientific Reports

doi: 10.1038/s41598-017-17561-1

Plasma levels of inflammatory biomarkers and leukocyte counts in patients undergoing cardiac surgery with CPB. Levels of soluble thrombomodulin (sCD141, ( a ) short-CPB (Admission n = 20; Post-op n = 18; d1 n = 20; d3 n = 19; d5 n = 17; d8 n = 13); long-CPB (Admission n = 22; Post-op n = 14; d1 n = 20; d3 n = 19; d5 n = 21; d8 n = 15)), ICAM-1 ( b) short-CPB (Admission n = 15; Post-op n = 12; d1 n = 13; d3 n = 15; d5 n = 14; d8 n = 11); long-CPB (Admission n = 14; Post-op n = 11; d1 n = 13; d3 n = 16; d5 n = 16; d8 n = 15)) and IL-6 ( c ) short-CPB (Admission n = 19; Post-op n = 18; d1 n = 20; d3 n = 21; d5 n = 20; d8 n = 14); long-CPB (Admission n = 20; Post-op n = 16; d1 n = 21; d3 n = 21; d5 n = 22; d8 n = 20)) were quantified in patients’ plasma by commercially available Elisas at the times indicated. CRP levels ( d) short-CPB (Admission n = 22; d1 n = 22; d3 n = 20; d5 n = 20; d8 n = 16); long-CPB (Admission n = 26; d1 n = 26; d3 n = 26; d5 n = 26; d8 n = 25)) and leukocyte counts ( e ) short-CPB (Admission n = 22; d1 n = 22; d3 n = 22; d5 n = 21; d8 n = 18); long-CPB (Admission n = 26; d1 n = 26; d3 n = 26; d5 n = 26; d8 n = 25)) were measured routinely in all patients. *p
Figure Legend Snippet: Plasma levels of inflammatory biomarkers and leukocyte counts in patients undergoing cardiac surgery with CPB. Levels of soluble thrombomodulin (sCD141, ( a ) short-CPB (Admission n = 20; Post-op n = 18; d1 n = 20; d3 n = 19; d5 n = 17; d8 n = 13); long-CPB (Admission n = 22; Post-op n = 14; d1 n = 20; d3 n = 19; d5 n = 21; d8 n = 15)), ICAM-1 ( b) short-CPB (Admission n = 15; Post-op n = 12; d1 n = 13; d3 n = 15; d5 n = 14; d8 n = 11); long-CPB (Admission n = 14; Post-op n = 11; d1 n = 13; d3 n = 16; d5 n = 16; d8 n = 15)) and IL-6 ( c ) short-CPB (Admission n = 19; Post-op n = 18; d1 n = 20; d3 n = 21; d5 n = 20; d8 n = 14); long-CPB (Admission n = 20; Post-op n = 16; d1 n = 21; d3 n = 21; d5 n = 22; d8 n = 20)) were quantified in patients’ plasma by commercially available Elisas at the times indicated. CRP levels ( d) short-CPB (Admission n = 22; d1 n = 22; d3 n = 20; d5 n = 20; d8 n = 16); long-CPB (Admission n = 26; d1 n = 26; d3 n = 26; d5 n = 26; d8 n = 25)) and leukocyte counts ( e ) short-CPB (Admission n = 22; d1 n = 22; d3 n = 22; d5 n = 21; d8 n = 18); long-CPB (Admission n = 26; d1 n = 26; d3 n = 26; d5 n = 26; d8 n = 25)) were measured routinely in all patients. *p

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    Change in median levels of serum inflammatory markers over time in patients who received infliximab 3 mg/kg + MTX or placebo + MTX through week 14 with a crossover to infliximab 6 mg/kg + MTX for <t>ICAM-1</t> (A), IL-6 (B), VEGF (C), MMP-3 (D), CRP (E), and IL-12p40 (F) . MTX, methotrexate; ICAM-1, intracellular cell adhesion molecule-1; IL-6, interleukin-6; VEGF, vascular endothelial growth factor; MMP-3, matrix metalloproteinase-3; CRP, C-reactive protein; IL-12p40, interleukin 12.
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    TNF-α induces <t>ICAM-1</t> expression via a PKCδ signaling in human RPECs. (A) Cells were pretreated with Ro318220, Rottlerin, or Gӧ6976 for 1 h, and then incubated with TNF-α for 6 h. The protein expression of ICAM-1 was determined by Western blot. (B) Cells were pretreated with Ro318220 (10 μM), Rottlerin (1 μM), or Gӧ6976 (10 μM) for 1 h, and then incubated with TNF-α for 4 h or 6 h. The mRNA levels and promoter activity of ICAM-1 were determined by real-time PCR and promoter assay, respectively. (C) Cells were pretreated without or with Rottlerin for 1 h, and then incubated with TNF-α for the indicated time intervals. The levels of phospho-PKCδ were determined by Western blot. Data are expressed as mean±S.E.M. of three independent experiments. * P
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    Soluble intercellular adhesion molecule (sICAM) in serum with e-cigarette (e-cig) inhalation. A : time course of <t>ICAM-1</t> in the serum of all subjects post-e-cig vaping, as assayed using quantitative ELISA. ICAM-1 was quantified using reference curves of standards provided by the manufacturer (R D Biosystems). B : average ICAM levels in blood post-e-cig inhalation across all 10 subjects (S1–S10). Data in the form of means ± SD of ICAM refer to samples obtained from 10 subjects for different time points. ICAM-1 levels are expressed as n -fold increase above baseline (i.e., pre-inhalation levels normalized to 1). * P
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    Change in median levels of serum inflammatory markers over time in patients who received infliximab 3 mg/kg + MTX or placebo + MTX through week 14 with a crossover to infliximab 6 mg/kg + MTX for ICAM-1 (A), IL-6 (B), VEGF (C), MMP-3 (D), CRP (E), and IL-12p40 (F) . MTX, methotrexate; ICAM-1, intracellular cell adhesion molecule-1; IL-6, interleukin-6; VEGF, vascular endothelial growth factor; MMP-3, matrix metalloproteinase-3; CRP, C-reactive protein; IL-12p40, interleukin 12.

    Journal: Pediatric Rheumatology Online Journal

    Article Title: The effect of infliximab plus methotrexate on the modulation of inflammatory disease markers in juvenile idiopathic arthritis: analyses from a randomized, placebo-controlled trial

    doi: 10.1186/1546-0096-8-24

    Figure Lengend Snippet: Change in median levels of serum inflammatory markers over time in patients who received infliximab 3 mg/kg + MTX or placebo + MTX through week 14 with a crossover to infliximab 6 mg/kg + MTX for ICAM-1 (A), IL-6 (B), VEGF (C), MMP-3 (D), CRP (E), and IL-12p40 (F) . MTX, methotrexate; ICAM-1, intracellular cell adhesion molecule-1; IL-6, interleukin-6; VEGF, vascular endothelial growth factor; MMP-3, matrix metalloproteinase-3; CRP, C-reactive protein; IL-12p40, interleukin 12.

    Article Snippet: Biomarker assessments Plasma levels of IL-6 and serum levels of MMP-3, ICAM-1, IL-12p40, and VEGF were measured using enzyme-linked immunosorbent assay (ELISA) kits (R & D Systems, Minneapolis, MN).

    Techniques:

    ATG7 knockdown inhibits thrombin-mediated expression of inflammatory proteins and NF-κB activity. HPAEC were transfected with si-Con or si-ATG7 for 48 h and then treated with thrombin (5 U/ml) for 6 h. ( A , B ) Conditioned media was collected from the cells and ELISAs were performed for ( A ) IL-6, ( B ) MCP-1. Error bars represent mean ± S.E. (n = 5 for each condition). ( C D ) Cell lysates were analyzed by ELISA for ( C ) ICAM-1 and ( D ) VCAM-1 levels. Error bars represent mean ± S.E. (n = 5 for each condition). ( E ) HPAEC were transfected with si-Con or si-ATG7 for 24 h, then transfected with NF-κBLUC and Renilla LUC constructs as described in the “ Materials and Methods ”. The cells were then treated with thrombin (5 U/ml) for 6 h and cell extracts were assayed for Firefly and Renilla luciferase activities. Renilla luciferase was used as an internal control for transfection efficiency. Error bars represent mean ± S.E. (n = 6 for each condition).

    Journal: Scientific Reports

    Article Title: Autophagy protein ATG7 is a critical regulator of endothelial cell inflammation and permeability

    doi: 10.1038/s41598-020-70126-7

    Figure Lengend Snippet: ATG7 knockdown inhibits thrombin-mediated expression of inflammatory proteins and NF-κB activity. HPAEC were transfected with si-Con or si-ATG7 for 48 h and then treated with thrombin (5 U/ml) for 6 h. ( A , B ) Conditioned media was collected from the cells and ELISAs were performed for ( A ) IL-6, ( B ) MCP-1. Error bars represent mean ± S.E. (n = 5 for each condition). ( C D ) Cell lysates were analyzed by ELISA for ( C ) ICAM-1 and ( D ) VCAM-1 levels. Error bars represent mean ± S.E. (n = 5 for each condition). ( E ) HPAEC were transfected with si-Con or si-ATG7 for 24 h, then transfected with NF-κBLUC and Renilla LUC constructs as described in the “ Materials and Methods ”. The cells were then treated with thrombin (5 U/ml) for 6 h and cell extracts were assayed for Firefly and Renilla luciferase activities. Renilla luciferase was used as an internal control for transfection efficiency. Error bars represent mean ± S.E. (n = 6 for each condition).

    Article Snippet: ELISAThe levels of IL-6, MCP-1, ICAM-1 and VCAM-1 in HPAEC were determined using ELISA kits from R & D Systems (Minneapolis, MN) according to manufacturers’ recommendations.

    Techniques: Expressing, Activity Assay, Transfection, Enzyme-linked Immunosorbent Assay, Construct, Luciferase

    TNF-α induces ICAM-1 expression via a PKCδ signaling in human RPECs. (A) Cells were pretreated with Ro318220, Rottlerin, or Gӧ6976 for 1 h, and then incubated with TNF-α for 6 h. The protein expression of ICAM-1 was determined by Western blot. (B) Cells were pretreated with Ro318220 (10 μM), Rottlerin (1 μM), or Gӧ6976 (10 μM) for 1 h, and then incubated with TNF-α for 4 h or 6 h. The mRNA levels and promoter activity of ICAM-1 were determined by real-time PCR and promoter assay, respectively. (C) Cells were pretreated without or with Rottlerin for 1 h, and then incubated with TNF-α for the indicated time intervals. The levels of phospho-PKCδ were determined by Western blot. Data are expressed as mean±S.E.M. of three independent experiments. * P

    Journal: PLoS ONE

    Article Title: TNF-α Mediates PKCδ/JNK1/2/c-Jun-Dependent Monocyte Adhesion via ICAM-1 Induction in Human Retinal Pigment Epithelial Cells

    doi: 10.1371/journal.pone.0117911

    Figure Lengend Snippet: TNF-α induces ICAM-1 expression via a PKCδ signaling in human RPECs. (A) Cells were pretreated with Ro318220, Rottlerin, or Gӧ6976 for 1 h, and then incubated with TNF-α for 6 h. The protein expression of ICAM-1 was determined by Western blot. (B) Cells were pretreated with Ro318220 (10 μM), Rottlerin (1 μM), or Gӧ6976 (10 μM) for 1 h, and then incubated with TNF-α for 4 h or 6 h. The mRNA levels and promoter activity of ICAM-1 were determined by real-time PCR and promoter assay, respectively. (C) Cells were pretreated without or with Rottlerin for 1 h, and then incubated with TNF-α for the indicated time intervals. The levels of phospho-PKCδ were determined by Western blot. Data are expressed as mean±S.E.M. of three independent experiments. * P

    Article Snippet: Anti-TNFR neutralizing antibody, anti-ICAM-1 neutralizing antibody, and TNF-α were from R & D Systems (Minneapolis, MN).

    Techniques: Expressing, Incubation, Western Blot, Activity Assay, Real-time Polymerase Chain Reaction, Promoter Assay

    TNF-α induces ICAM-1 expression and monocyte adhesion. (A) Human RPECs were incubated with TNF-α for the indicated time intervals. The protein expression of ICAM-1 was determined by Western blot. (B, C) Cells were incubated with TNF-α (15 ng/ml) for the indicated time intervals. The mRNA levels and promoter activity of ICAM-1 were determined by real-time PCR and promoter assay, respectively. (D) RPECs were pretreated with an ICAM-1 neutralizing antibody for 1 h, and then incubated with TNF-α for 6 h. The THP-1 cells adherence was measured. Data are expressed as mean±S.E.M. of three independent experiments. * P

    Journal: PLoS ONE

    Article Title: TNF-α Mediates PKCδ/JNK1/2/c-Jun-Dependent Monocyte Adhesion via ICAM-1 Induction in Human Retinal Pigment Epithelial Cells

    doi: 10.1371/journal.pone.0117911

    Figure Lengend Snippet: TNF-α induces ICAM-1 expression and monocyte adhesion. (A) Human RPECs were incubated with TNF-α for the indicated time intervals. The protein expression of ICAM-1 was determined by Western blot. (B, C) Cells were incubated with TNF-α (15 ng/ml) for the indicated time intervals. The mRNA levels and promoter activity of ICAM-1 were determined by real-time PCR and promoter assay, respectively. (D) RPECs were pretreated with an ICAM-1 neutralizing antibody for 1 h, and then incubated with TNF-α for 6 h. The THP-1 cells adherence was measured. Data are expressed as mean±S.E.M. of three independent experiments. * P

    Article Snippet: Anti-TNFR neutralizing antibody, anti-ICAM-1 neutralizing antibody, and TNF-α were from R & D Systems (Minneapolis, MN).

    Techniques: Expressing, Incubation, Western Blot, Activity Assay, Real-time Polymerase Chain Reaction, Promoter Assay

    TNF-α induces ICAM-1 expression via a PKCδ/JNK1/2 signaling in human RPECs. (A) Cells were pretreated with U0126, SP600125, or SB202190 for 1 h, and then incubated with TNF-α for 6 h. The protein expression of ICAM-1 was determined by Western blot. (B) Cells were transfected with siRNA of scrambled, JNK2, or p42, and then incubated with TNF-α for 6 h. The protein levels of p42, JNK2, and ICAM-1 were determined by Western blot. (C) Cells were pretreated with U0126 (10 μM), SP600125 (10 μM), or SB202190 (10 μM) for 1 h, and then incubated with TNF-α for 4 h or 6 h. The mRNA levels and promoter activity of ICAM-1 were determined by real-time PCR and promoter assay, respectively. (D) Cells were pretreated without or with U0126 or SP600125 for 1 h, and then incubated with TNF-α for the indicated times. The levels of phospho-p42/p44 MAPK and phospho-JNK1/2 were determined by Western blot. (E) Cells were pretreated without or with Rottlerin for 1 h, and then incubated with TNF-α for the indicated time intervals. The levels of phospho-p42/p44 MAPK and phospho-JNK1/2 were determined by Western blot. (F) RPECs were pretreated with Ro318220, Rottlerin, SP600125, or U0126 for 1 h, and then incubated with TNF-α for 6 h. The THP-1 cells adherence was measured. Data are expressed as mean±S.E.M. of three independent experiments. * P

    Journal: PLoS ONE

    Article Title: TNF-α Mediates PKCδ/JNK1/2/c-Jun-Dependent Monocyte Adhesion via ICAM-1 Induction in Human Retinal Pigment Epithelial Cells

    doi: 10.1371/journal.pone.0117911

    Figure Lengend Snippet: TNF-α induces ICAM-1 expression via a PKCδ/JNK1/2 signaling in human RPECs. (A) Cells were pretreated with U0126, SP600125, or SB202190 for 1 h, and then incubated with TNF-α for 6 h. The protein expression of ICAM-1 was determined by Western blot. (B) Cells were transfected with siRNA of scrambled, JNK2, or p42, and then incubated with TNF-α for 6 h. The protein levels of p42, JNK2, and ICAM-1 were determined by Western blot. (C) Cells were pretreated with U0126 (10 μM), SP600125 (10 μM), or SB202190 (10 μM) for 1 h, and then incubated with TNF-α for 4 h or 6 h. The mRNA levels and promoter activity of ICAM-1 were determined by real-time PCR and promoter assay, respectively. (D) Cells were pretreated without or with U0126 or SP600125 for 1 h, and then incubated with TNF-α for the indicated times. The levels of phospho-p42/p44 MAPK and phospho-JNK1/2 were determined by Western blot. (E) Cells were pretreated without or with Rottlerin for 1 h, and then incubated with TNF-α for the indicated time intervals. The levels of phospho-p42/p44 MAPK and phospho-JNK1/2 were determined by Western blot. (F) RPECs were pretreated with Ro318220, Rottlerin, SP600125, or U0126 for 1 h, and then incubated with TNF-α for 6 h. The THP-1 cells adherence was measured. Data are expressed as mean±S.E.M. of three independent experiments. * P

    Article Snippet: Anti-TNFR neutralizing antibody, anti-ICAM-1 neutralizing antibody, and TNF-α were from R & D Systems (Minneapolis, MN).

    Techniques: Expressing, Incubation, Western Blot, Transfection, Activity Assay, Real-time Polymerase Chain Reaction, Promoter Assay

    Schematic representation of the signaling pathways involved in the TNF-α-induced ICAM-1 expression in RPECs. TNF-α-induced ICAM-1 expression and monocyte adhesion are mediated through a TNFR1/TRAF2/PKCδ/JNK1/2/c-Jun signaling pathway in human RPECs.

    Journal: PLoS ONE

    Article Title: TNF-α Mediates PKCδ/JNK1/2/c-Jun-Dependent Monocyte Adhesion via ICAM-1 Induction in Human Retinal Pigment Epithelial Cells

    doi: 10.1371/journal.pone.0117911

    Figure Lengend Snippet: Schematic representation of the signaling pathways involved in the TNF-α-induced ICAM-1 expression in RPECs. TNF-α-induced ICAM-1 expression and monocyte adhesion are mediated through a TNFR1/TRAF2/PKCδ/JNK1/2/c-Jun signaling pathway in human RPECs.

    Article Snippet: Anti-TNFR neutralizing antibody, anti-ICAM-1 neutralizing antibody, and TNF-α were from R & D Systems (Minneapolis, MN).

    Techniques: Expressing

    TNF-α induces ICAM-1 expression through a c-Jun pathway. (A) Human RPECs were pretreated with Tanshinone IIA for 1 h, and then incubated with TNF-α for 6 h. The protein expression of ICAM-1 was determined by Western blot. (B) Cells were pretreated with Tanshinone IIA (10 μM) for 1 h, and then incubated with TNF-α for 4 h or 6 h. The mRNA levels and promoter activity of ICAM-1 were determined by real-time PCR and promoter assay, respectively. (C) Cells were transfected with wild-type ICAM-1 promoter-luciferaase or mutant ICAM-1 promoter-luciferaase (ΔAP-1), and then incubated with TNF-α (15 ng/ml) for 6 h. The ICAM-1 promoter activity was determined in the cell lysates. (D) Cells were transfected with siRNA of scrambled or c-Jun, and then incubated with TNF-α for 6 h. The protein levels of c-Jun and ICAM-1 were determined by Western blot. (E) Cells were pretreated without or with Rottlerin or SP600125 for 1 h, and then incubated with TNF-α for the indicated time intervals. The levels of phospho-c-Jun were determined by Western blot. (F) RPECs were pretreated with Tanshinone IIA for 1 h, and then incubated with TNF-α for 6 h. The THP-1 cells adherence was measured. Data are expressed as mean±S.E.M. of three independent experiments. * P

    Journal: PLoS ONE

    Article Title: TNF-α Mediates PKCδ/JNK1/2/c-Jun-Dependent Monocyte Adhesion via ICAM-1 Induction in Human Retinal Pigment Epithelial Cells

    doi: 10.1371/journal.pone.0117911

    Figure Lengend Snippet: TNF-α induces ICAM-1 expression through a c-Jun pathway. (A) Human RPECs were pretreated with Tanshinone IIA for 1 h, and then incubated with TNF-α for 6 h. The protein expression of ICAM-1 was determined by Western blot. (B) Cells were pretreated with Tanshinone IIA (10 μM) for 1 h, and then incubated with TNF-α for 4 h or 6 h. The mRNA levels and promoter activity of ICAM-1 were determined by real-time PCR and promoter assay, respectively. (C) Cells were transfected with wild-type ICAM-1 promoter-luciferaase or mutant ICAM-1 promoter-luciferaase (ΔAP-1), and then incubated with TNF-α (15 ng/ml) for 6 h. The ICAM-1 promoter activity was determined in the cell lysates. (D) Cells were transfected with siRNA of scrambled or c-Jun, and then incubated with TNF-α for 6 h. The protein levels of c-Jun and ICAM-1 were determined by Western blot. (E) Cells were pretreated without or with Rottlerin or SP600125 for 1 h, and then incubated with TNF-α for the indicated time intervals. The levels of phospho-c-Jun were determined by Western blot. (F) RPECs were pretreated with Tanshinone IIA for 1 h, and then incubated with TNF-α for 6 h. The THP-1 cells adherence was measured. Data are expressed as mean±S.E.M. of three independent experiments. * P

    Article Snippet: Anti-TNFR neutralizing antibody, anti-ICAM-1 neutralizing antibody, and TNF-α were from R & D Systems (Minneapolis, MN).

    Techniques: Expressing, Incubation, Western Blot, Activity Assay, Real-time Polymerase Chain Reaction, Promoter Assay, Transfection, Mutagenesis

    TNF-α-induced ICAM-1 expression is mediated via the formation of a TNFR1/TRAF2 complex. (A) Human RPECs were pretreated with a TNFR neutralizing antibody, and then incubated with TNF-α for 6 h. The protein expression of ICAM-1 was determined by Western blot. (B) RPECs were pretreated with the neutralizing antibody of TNFR for 1 h, and then incubated with TNF-α for 6 h. The THP-1 cells adherence was measured. (C) Cells were transfected with siRNA of scrambled, TNFR1, or TRAF2, and then incubated with TNF-α for 6 h. The protein levels of TNFR1, TRAF2, and ICAM-1 were determined by Western blot. (D) Cells were incubated with TNF-α (15 ng/ml) for various time intervals. The cell lysates were subjected to immunoprecipitation using an anti-TRAF2 antibody, and then the immunoprecipitates were analyzed by Western blot using an anti-TRAF2 or anti-TNFR1 antibody. (E) Cells were treated without or with TNF-α for 6 h. The expression of TNFR1 was determined. Data are expressed as mean±S.E.M. of three independent experiments. * P

    Journal: PLoS ONE

    Article Title: TNF-α Mediates PKCδ/JNK1/2/c-Jun-Dependent Monocyte Adhesion via ICAM-1 Induction in Human Retinal Pigment Epithelial Cells

    doi: 10.1371/journal.pone.0117911

    Figure Lengend Snippet: TNF-α-induced ICAM-1 expression is mediated via the formation of a TNFR1/TRAF2 complex. (A) Human RPECs were pretreated with a TNFR neutralizing antibody, and then incubated with TNF-α for 6 h. The protein expression of ICAM-1 was determined by Western blot. (B) RPECs were pretreated with the neutralizing antibody of TNFR for 1 h, and then incubated with TNF-α for 6 h. The THP-1 cells adherence was measured. (C) Cells were transfected with siRNA of scrambled, TNFR1, or TRAF2, and then incubated with TNF-α for 6 h. The protein levels of TNFR1, TRAF2, and ICAM-1 were determined by Western blot. (D) Cells were incubated with TNF-α (15 ng/ml) for various time intervals. The cell lysates were subjected to immunoprecipitation using an anti-TRAF2 antibody, and then the immunoprecipitates were analyzed by Western blot using an anti-TRAF2 or anti-TNFR1 antibody. (E) Cells were treated without or with TNF-α for 6 h. The expression of TNFR1 was determined. Data are expressed as mean±S.E.M. of three independent experiments. * P

    Article Snippet: Anti-TNFR neutralizing antibody, anti-ICAM-1 neutralizing antibody, and TNF-α were from R & D Systems (Minneapolis, MN).

    Techniques: Expressing, Incubation, Western Blot, Transfection, Immunoprecipitation

    Soluble intercellular adhesion molecule (sICAM) in serum with e-cigarette (e-cig) inhalation. A : time course of ICAM-1 in the serum of all subjects post-e-cig vaping, as assayed using quantitative ELISA. ICAM-1 was quantified using reference curves of standards provided by the manufacturer (R D Biosystems). B : average ICAM levels in blood post-e-cig inhalation across all 10 subjects (S1–S10). Data in the form of means ± SD of ICAM refer to samples obtained from 10 subjects for different time points. ICAM-1 levels are expressed as n -fold increase above baseline (i.e., pre-inhalation levels normalized to 1). * P

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: Acute exposure to e-cigarettes causes inflammation and pulmonary endothelial oxidative stress in nonsmoking, healthy young subjects

    doi: 10.1152/ajplung.00110.2019

    Figure Lengend Snippet: Soluble intercellular adhesion molecule (sICAM) in serum with e-cigarette (e-cig) inhalation. A : time course of ICAM-1 in the serum of all subjects post-e-cig vaping, as assayed using quantitative ELISA. ICAM-1 was quantified using reference curves of standards provided by the manufacturer (R D Biosystems). B : average ICAM levels in blood post-e-cig inhalation across all 10 subjects (S1–S10). Data in the form of means ± SD of ICAM refer to samples obtained from 10 subjects for different time points. ICAM-1 levels are expressed as n -fold increase above baseline (i.e., pre-inhalation levels normalized to 1). * P

    Article Snippet: CRP and ICAM-1 were detected using commercially available kits (Quantikine R & D Systems, Minneapolis, MN).

    Techniques: Enzyme-linked Immunosorbent Assay