Structured Review

Bio-Rad icam 1
Effect of Pom on MHC-I (HLA-A, B and C), ICAM and B7-2 mRNA gene expression in BCBL-1 cells induced with butyrate BCBL-1 cells were treated with control (DMSO) or Pom (1 μM) for 24 h followed by treatment with PBS or butyrate for an additional 24 h. Total mRNA was isolated and analyzed for expression levels by real time QT-PCR and was normalized to 18S levels. Shown are the fold changes in mRNA expression for total A . HLA and HLA A, B and C alleles following treatment and B . <t>ICAM-1</t> and B7-2. Values are the average +/- standard deviation of four independent experiments. *** P
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Images

1) Product Images from "Restoration of immune surface molecules in Kaposi sarcoma-associated herpes virus infected cells by lenalidomide and pomalidomide"

Article Title: Restoration of immune surface molecules in Kaposi sarcoma-associated herpes virus infected cells by lenalidomide and pomalidomide

Journal: Oncotarget

doi: 10.18632/oncotarget.17960

Effect of Pom on MHC-I (HLA-A, B and C), ICAM and B7-2 mRNA gene expression in BCBL-1 cells induced with butyrate BCBL-1 cells were treated with control (DMSO) or Pom (1 μM) for 24 h followed by treatment with PBS or butyrate for an additional 24 h. Total mRNA was isolated and analyzed for expression levels by real time QT-PCR and was normalized to 18S levels. Shown are the fold changes in mRNA expression for total A . HLA and HLA A, B and C alleles following treatment and B . ICAM-1 and B7-2. Values are the average +/- standard deviation of four independent experiments. *** P
Figure Legend Snippet: Effect of Pom on MHC-I (HLA-A, B and C), ICAM and B7-2 mRNA gene expression in BCBL-1 cells induced with butyrate BCBL-1 cells were treated with control (DMSO) or Pom (1 μM) for 24 h followed by treatment with PBS or butyrate for an additional 24 h. Total mRNA was isolated and analyzed for expression levels by real time QT-PCR and was normalized to 18S levels. Shown are the fold changes in mRNA expression for total A . HLA and HLA A, B and C alleles following treatment and B . ICAM-1 and B7-2. Values are the average +/- standard deviation of four independent experiments. *** P

Techniques Used: Expressing, Isolation, Polymerase Chain Reaction, Standard Deviation

Restoration of ICAM-1 and B7-2 but not ICAM-3 expression in BCBL-1 cells treated with Pom A . ICAM-1 expression in BCBL-1 cells and in B . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). C . B7-2 expression in BCBL-1 cells and in D . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). E . ICAM-3 expression in BCBL-1 cells and in F . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). The data shows a representative experiment of four independent experiments for A . and C . and two independent experiments for B ., D ., and F . with similar results. The grey shading shows the isotype control.
Figure Legend Snippet: Restoration of ICAM-1 and B7-2 but not ICAM-3 expression in BCBL-1 cells treated with Pom A . ICAM-1 expression in BCBL-1 cells and in B . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). C . B7-2 expression in BCBL-1 cells and in D . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). E . ICAM-3 expression in BCBL-1 cells and in F . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). The data shows a representative experiment of four independent experiments for A . and C . and two independent experiments for B ., D ., and F . with similar results. The grey shading shows the isotype control.

Techniques Used: Expressing, FACS

Effect of Len on ICAM-1 and B7-2 expression in BCBL-1 cells, effect of Pom on MHC-II expression in BCBL-1 and BJAB cells, and effect of Pom on ICAM-1 and B7-2 in JSC-1 cells A . ICAM-1 expression and B . B7-2 expression in BCBL-1 cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. C . ICAM-1 expression D . B7-2 expression in JSC-1 cells pretreated for 48 h with DMSO vehicle control or Pom (0.2 μM) as determined by FACS. E . MHC-II expression in BCBL-1 cells or F . BJAB cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. The data is representative of two independent experiments in A, one experiment in B-D, and two experiments in E and F. The grey shading shows the isotype control.
Figure Legend Snippet: Effect of Len on ICAM-1 and B7-2 expression in BCBL-1 cells, effect of Pom on MHC-II expression in BCBL-1 and BJAB cells, and effect of Pom on ICAM-1 and B7-2 in JSC-1 cells A . ICAM-1 expression and B . B7-2 expression in BCBL-1 cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. C . ICAM-1 expression D . B7-2 expression in JSC-1 cells pretreated for 48 h with DMSO vehicle control or Pom (0.2 μM) as determined by FACS. E . MHC-II expression in BCBL-1 cells or F . BJAB cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. The data is representative of two independent experiments in A, one experiment in B-D, and two experiments in E and F. The grey shading shows the isotype control.

Techniques Used: Expressing, FACS

2) Product Images from "Ischaemia-reperfusion injury in orthotopic mouse lung transplants - a scanning electron microscopy study"

Article Title: Ischaemia-reperfusion injury in orthotopic mouse lung transplants - a scanning electron microscopy study

Journal: International Journal of Experimental Pathology

doi: 10.1111/j.1365-2613.2010.00752.x

Immunohistochemical staining of ICAM-1. Non-transplanted lungs show a fine lining of ICAM-expression on the endothelium of the vessel. In contrast, transplanted lungs that were exposed to 2 h of ischaemia and 30 min of reperfusion, the endothelium increasingly
Figure Legend Snippet: Immunohistochemical staining of ICAM-1. Non-transplanted lungs show a fine lining of ICAM-expression on the endothelium of the vessel. In contrast, transplanted lungs that were exposed to 2 h of ischaemia and 30 min of reperfusion, the endothelium increasingly

Techniques Used: Immunohistochemistry, Staining, Expressing

3) Product Images from "Immunoprivileged status of the liver is controlled by Toll-like receptor 3 signaling"

Article Title: Immunoprivileged status of the liver is controlled by Toll-like receptor 3 signaling

Journal:

doi: 10.1172/JCI28349

Activation of TLR3 and regulation of Icam-1 , Vcam-1 , and Cxcl9 .
Figure Legend Snippet: Activation of TLR3 and regulation of Icam-1 , Vcam-1 , and Cxcl9 .

Techniques Used: Activation Assay

4) Product Images from "The Effects of Subacute Inhaled Multi-Walled Carbon Nanotube Exposure on Signaling Pathways Associated with Cholesterol Transport and Inflammatory Markers in the Vasculature of Wild-Type Mice."

Article Title: The Effects of Subacute Inhaled Multi-Walled Carbon Nanotube Exposure on Signaling Pathways Associated with Cholesterol Transport and Inflammatory Markers in the Vasculature of Wild-Type Mice.

Journal: Toxicology letters

doi: 10.1016/j.toxlet.2018.08.004

Expression of biomarkers of coronary artery disease in MWCNT vs. filtered-air exposed C57Bl/6 mice. RT-qPCR analysis of (A) ICAM-1 mRNA; (B) VCAM-1 mRNA; (C) ET-1 mRNA; (D) TNF-α mRNA; (E) IL-16 mRNA; and (F) IL-1β mRNA expression between filtered air (FA)-CT and MWCNT-exposed mice. Data reported as mean normalized gene expression to GAPDH reference gene. An n=7 per group was used to analyze each gene of interest. *p
Figure Legend Snippet: Expression of biomarkers of coronary artery disease in MWCNT vs. filtered-air exposed C57Bl/6 mice. RT-qPCR analysis of (A) ICAM-1 mRNA; (B) VCAM-1 mRNA; (C) ET-1 mRNA; (D) TNF-α mRNA; (E) IL-16 mRNA; and (F) IL-1β mRNA expression between filtered air (FA)-CT and MWCNT-exposed mice. Data reported as mean normalized gene expression to GAPDH reference gene. An n=7 per group was used to analyze each gene of interest. *p

Techniques Used: Expressing, Mouse Assay, Quantitative RT-PCR

5) Product Images from "Biological function of CD40 on human endothelial cells: costimulation with CD40 ligand and interleukin-4 selectively induces expression of vascular cell adhesion molecule-1 and P-selectin resulting in preferential adhesion of lymphocytes"

Article Title: Biological function of CD40 on human endothelial cells: costimulation with CD40 ligand and interleukin-4 selectively induces expression of vascular cell adhesion molecule-1 and P-selectin resulting in preferential adhesion of lymphocytes

Journal: Immunology

doi: 10.1046/j.1365-2567.2000.00061.x

Regulation of adhesion molecule expression on endothelial cells by interleukin (IL)-4 and CD40 ligand (CD40L). Human umbilical vein endothelial cell (HUVEC) monolayers were stimulated for the times indicated with medium alone (•), or with 100 U/ml of IL-4 (▪), 1 ng/ml CD40L (▴) or a combination of IL-4 and CD40L (▾). Expression of adhesion molecules P-selectin (a), ICAM-1 (b) and E-selectin (c) was determined by flow cytometry and expressed as mean fluorescence intensity (MFI). These experiments were repeated at least five times, always with the same result. The data presented is from a representative experiment in each case.
Figure Legend Snippet: Regulation of adhesion molecule expression on endothelial cells by interleukin (IL)-4 and CD40 ligand (CD40L). Human umbilical vein endothelial cell (HUVEC) monolayers were stimulated for the times indicated with medium alone (•), or with 100 U/ml of IL-4 (▪), 1 ng/ml CD40L (▴) or a combination of IL-4 and CD40L (▾). Expression of adhesion molecules P-selectin (a), ICAM-1 (b) and E-selectin (c) was determined by flow cytometry and expressed as mean fluorescence intensity (MFI). These experiments were repeated at least five times, always with the same result. The data presented is from a representative experiment in each case.

Techniques Used: Expressing, Flow Cytometry, Cytometry, Fluorescence

6) Product Images from "Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model"

Article Title: Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model

Journal: Stroke Research and Treatment

doi: 10.4061/2011/846716

Western blot analysis of phosphorylated ERK1/2 and ICAM-1. (a) Phosphorylation of ERK1/2 was significantly higher in hypothermic (33) brains than normothermic (37) ones at 15, 30, and 120 minutes after ischemic insult ( n = 6 per group). Total ERK1/2 level was not changed. (b) Ischemia-induced increase of ICAM-1 at 24 hours after MCAO was suppressed by hypothermia. But this suppression was not observed when ERK1/2 inhibition was done (U0126, n = 4) at the dose which almost completely inhibited ERK1/2 phosphorylation. * P
Figure Legend Snippet: Western blot analysis of phosphorylated ERK1/2 and ICAM-1. (a) Phosphorylation of ERK1/2 was significantly higher in hypothermic (33) brains than normothermic (37) ones at 15, 30, and 120 minutes after ischemic insult ( n = 6 per group). Total ERK1/2 level was not changed. (b) Ischemia-induced increase of ICAM-1 at 24 hours after MCAO was suppressed by hypothermia. But this suppression was not observed when ERK1/2 inhibition was done (U0126, n = 4) at the dose which almost completely inhibited ERK1/2 phosphorylation. * P

Techniques Used: Western Blot, Inhibition

7) Product Images from "Inhibitory Effect of Melanoma Differentiation Associated Gene-7/Interleukin-24 on Invasion In Vitro of Human Melanoma Cancer Cells"

Article Title: Inhibitory Effect of Melanoma Differentiation Associated Gene-7/Interleukin-24 on Invasion In Vitro of Human Melanoma Cancer Cells

Journal: Journal of Korean Medical Science

doi: 10.3346/jkms.2013.28.6.833

Effects of MDA-7 on expression of MMP-2/9, CDK1, ICAM-1 and PTEN in LiBr cell lines. ( A ) Western blot showed decreased MMP-2/9, CDK1 and ICAM-1 expression and increased PTEN expression on protein level in MDA-7 overexpressing LiBr cells. β-actin was used as an internal control for loading. The experiment shown is representative of three independent experiments with similar results. ( B ) Real-time PCR showed decreased MMP-2/9, CDK1 and ICAM-1 expression and increased PTEN expression on mRNA level in MDA-7 overexpressing LiBr cells. GAPDH was used as an internal control for loading. Bars mean±SD. * P > 0.05, † P
Figure Legend Snippet: Effects of MDA-7 on expression of MMP-2/9, CDK1, ICAM-1 and PTEN in LiBr cell lines. ( A ) Western blot showed decreased MMP-2/9, CDK1 and ICAM-1 expression and increased PTEN expression on protein level in MDA-7 overexpressing LiBr cells. β-actin was used as an internal control for loading. The experiment shown is representative of three independent experiments with similar results. ( B ) Real-time PCR showed decreased MMP-2/9, CDK1 and ICAM-1 expression and increased PTEN expression on mRNA level in MDA-7 overexpressing LiBr cells. GAPDH was used as an internal control for loading. Bars mean±SD. * P > 0.05, † P

Techniques Used: Multiple Displacement Amplification, Expressing, Western Blot, Real-time Polymerase Chain Reaction

8) Product Images from "Dengue Hemorrhagic Fever-Associated Immunomediators Induced via Maturation of Dengue Virus Nonstructural 4B Protein in Monocytes Modulate Endothelial Cell Adhesion Molecules and Human Microvascular Endothelial Cells Permeability"

Article Title: Dengue Hemorrhagic Fever-Associated Immunomediators Induced via Maturation of Dengue Virus Nonstructural 4B Protein in Monocytes Modulate Endothelial Cell Adhesion Molecules and Human Microvascular Endothelial Cells Permeability

Journal: Virology

doi: 10.1016/j.virol.2011.10.030

DENV-infected HMVEC do not increase expression of ICAM-1, VCAM-1 or E-sel nor increase permeability levels
Figure Legend Snippet: DENV-infected HMVEC do not increase expression of ICAM-1, VCAM-1 or E-sel nor increase permeability levels

Techniques Used: Infection, Expressing, Permeability

Supernatants from DENV-infected THP-1 cells increase HMVEC adhesion molecules and permeability. (A) qRT-PCR analysis of ICAM-1, VCAM-1 and E-sel mRNA fold-change in HMVEC treated for 16 h with supernatants from control or infected THP-1 cells collected
Figure Legend Snippet: Supernatants from DENV-infected THP-1 cells increase HMVEC adhesion molecules and permeability. (A) qRT-PCR analysis of ICAM-1, VCAM-1 and E-sel mRNA fold-change in HMVEC treated for 16 h with supernatants from control or infected THP-1 cells collected

Techniques Used: Infection, Permeability, Quantitative RT-PCR

Immunomediators secreted by THP-1 cells expressing 2KNS4B or NS5 proteins promote endothelial cell activation and permeability. (A) qRT-PCR analysis of ICAM-1, VCAM-1 and E-sel mRNA fold-change from HMVEC after treatment with supernatants from THP-1 cells
Figure Legend Snippet: Immunomediators secreted by THP-1 cells expressing 2KNS4B or NS5 proteins promote endothelial cell activation and permeability. (A) qRT-PCR analysis of ICAM-1, VCAM-1 and E-sel mRNA fold-change from HMVEC after treatment with supernatants from THP-1 cells

Techniques Used: Expressing, Activation Assay, Permeability, Quantitative RT-PCR

9) Product Images from "Failure of P-selectin blockade alone to protect the liver from ischemia-reperfusion injury in the isolated blood-perfused rat liver"

Article Title: Failure of P-selectin blockade alone to protect the liver from ischemia-reperfusion injury in the isolated blood-perfused rat liver

Journal: World Journal of Gastroenterology : WJG

doi: 10.3748/wjg.14.6808

Semi-quantitative RT-PCR analysis of P-selectin and ICAM-1 mRNA levels in isolated-blood-perfused control and P-selectin Ab-treated rat livers after 6 h of cold ischemia. a P
Figure Legend Snippet: Semi-quantitative RT-PCR analysis of P-selectin and ICAM-1 mRNA levels in isolated-blood-perfused control and P-selectin Ab-treated rat livers after 6 h of cold ischemia. a P

Techniques Used: Quantitative RT-PCR, Isolation

Western blot analysis of P-selectin and ICAM-1 protein levels in isolated-blood-perfused control and P-selectin Ab-treated rat livers after 6 h of cold ischemia.
Figure Legend Snippet: Western blot analysis of P-selectin and ICAM-1 protein levels in isolated-blood-perfused control and P-selectin Ab-treated rat livers after 6 h of cold ischemia.

Techniques Used: Western Blot, Isolation

10) Product Images from "Suppressive effects of methylthiouracil on polyphosphate‐mediated vascular inflammatory responses"

Article Title: Suppressive effects of methylthiouracil on polyphosphate‐mediated vascular inflammatory responses

Journal: Journal of Cellular and Molecular Medicine

doi: 10.1111/jcmm.12925

Effects of methylthiouracil ( MTU ) on the PolyP‐induced expression of cellular adhesion molecules ( CAM s) in human umbilical vein endothelial cells ( HUVEC s). ( A ) The PolyP‐mediated (50 μM) levels of expression of vascular cell adhesion molecule‐1 ( VCAM ‐1; white bar), intercellular adhesion molecule‐1 ( ICAM ‐1; grey bar), and E‐selectin (black bar) proteins in  HUVEC s were analysed with whole‐cell  ELISA  after treating the monolayers with  MTU . ( B ) The PolyP‐mediated (50 μM) levels of expression of  VCAM ‐1 (white bar),  ICAM ‐1 (grey bar), and E‐selectin (black bar) transcription (mRNA) in  HUVEC s were analysed with whole‐cell  ELISA  after treating the monolayers with  MTU . The results are expressed as the means ±  SEM  of three independent experiments. * P
Figure Legend Snippet: Effects of methylthiouracil ( MTU ) on the PolyP‐induced expression of cellular adhesion molecules ( CAM s) in human umbilical vein endothelial cells ( HUVEC s). ( A ) The PolyP‐mediated (50 μM) levels of expression of vascular cell adhesion molecule‐1 ( VCAM ‐1; white bar), intercellular adhesion molecule‐1 ( ICAM ‐1; grey bar), and E‐selectin (black bar) proteins in HUVEC s were analysed with whole‐cell ELISA after treating the monolayers with MTU . ( B ) The PolyP‐mediated (50 μM) levels of expression of VCAM ‐1 (white bar), ICAM ‐1 (grey bar), and E‐selectin (black bar) transcription (mRNA) in HUVEC s were analysed with whole‐cell ELISA after treating the monolayers with MTU . The results are expressed as the means ± SEM of three independent experiments. * P

Techniques Used: Expressing, Chick Chorioallantoic Membrane Assay, Enzyme-linked Immunosorbent Assay

11) Product Images from "Annexin A2 is involved in antiphospholipid antibody-mediated pathogenic effects in vitro and in vivo"

Article Title: Annexin A2 is involved in antiphospholipid antibody-mediated pathogenic effects in vitro and in vivo

Journal: Blood

doi: 10.1182/blood-2008-11-188698

Diagrammatic representation of interaction of aPL/anti-β 2 GPI Abs with β 2 GPI and receptor(s) on ECs . aPL/anti-β 2 GPI Abs bind to domain I (DI) of β 2 GPI. β 2 GPI anchors to annexin A2 on the surface of ECs, possibly through domain V (DV) of the protein. Annexin A2 does not have a transmembrane domain. Hence, it is not able to transduce intracellular signaling. Other membrane proteins (ie, TLR-4 or apoER2′) may act as accessory molecules or may bind β 2 GPI directly and induce phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) and translocation of nuclear factor-κB (NF-κB), leading to a proinflammatory/prothrombotic phenotype (up-regulation of tissue factor and cellular adhesion molecules [ie, E-sel, ICAM-1, VCAM-1]). Reprinted from Trends in Immunology , P. Meroni, N. Rhonda, E. Raschi, and M.O. Borghi, Humoral immunity against endothelium; theory or reality? 2005;26:275-281, with permission from Elsevier.
Figure Legend Snippet: Diagrammatic representation of interaction of aPL/anti-β 2 GPI Abs with β 2 GPI and receptor(s) on ECs . aPL/anti-β 2 GPI Abs bind to domain I (DI) of β 2 GPI. β 2 GPI anchors to annexin A2 on the surface of ECs, possibly through domain V (DV) of the protein. Annexin A2 does not have a transmembrane domain. Hence, it is not able to transduce intracellular signaling. Other membrane proteins (ie, TLR-4 or apoER2′) may act as accessory molecules or may bind β 2 GPI directly and induce phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) and translocation of nuclear factor-κB (NF-κB), leading to a proinflammatory/prothrombotic phenotype (up-regulation of tissue factor and cellular adhesion molecules [ie, E-sel, ICAM-1, VCAM-1]). Reprinted from Trends in Immunology , P. Meroni, N. Rhonda, E. Raschi, and M.O. Borghi, Humoral immunity against endothelium; theory or reality? 2005;26:275-281, with permission from Elsevier.

Techniques Used: Transduction, Activated Clotting Time Assay, Translocation Assay

Effect of anti-A2 on IgG-APS–induced expression of ICAM-1 and E-sel in HUVECs . HUVECs were cultured and treated with either 200 μg/mL IgG-APS or 200 μg/mL IgG-NHS in the presence or absence of 1 μg/mL anti-A2 IgG Ab or 1 μg/mL MuMoAbC, as indicated in “In vitro detection of surface E-sel and ICAM-1 on EC.” Some cells were treated with LPS, as a positive control, or with medium alone, as a negative control. ICAM-1 (A) and E-sel (B) expression were determined by cyto-ELISA, and the data expressed as means ± SD in O.D. units. Experiments were run in triplicate and performed 3 times. ¶Statistically different from medium-treated cells ( P = .001). *Statistically different from IgG-NHS–treated cells ( P = .001). **Statistically different from IgG-APS–treated cells (ICAM-1, P = .001; E-sel, P = .001).
Figure Legend Snippet: Effect of anti-A2 on IgG-APS–induced expression of ICAM-1 and E-sel in HUVECs . HUVECs were cultured and treated with either 200 μg/mL IgG-APS or 200 μg/mL IgG-NHS in the presence or absence of 1 μg/mL anti-A2 IgG Ab or 1 μg/mL MuMoAbC, as indicated in “In vitro detection of surface E-sel and ICAM-1 on EC.” Some cells were treated with LPS, as a positive control, or with medium alone, as a negative control. ICAM-1 (A) and E-sel (B) expression were determined by cyto-ELISA, and the data expressed as means ± SD in O.D. units. Experiments were run in triplicate and performed 3 times. ¶Statistically different from medium-treated cells ( P = .001). *Statistically different from IgG-NHS–treated cells ( P = .001). **Statistically different from IgG-APS–treated cells (ICAM-1, P = .001; E-sel, P = .001).

Techniques Used: Expressing, Cell Culture, Positive Control, Negative Control, Enzyme-linked Immunosorbent Assay

12) Product Images from "Long-term Efficacy of Intravenous Immunoglobulin Therapy for Moderate to Severe Childhood Atopic Dermatitis"

Article Title: Long-term Efficacy of Intravenous Immunoglobulin Therapy for Moderate to Severe Childhood Atopic Dermatitis

Journal: Allergy, Asthma & Immunology Research

doi: 10.4168/aair.2011.3.2.89

Intracellular cell adhesion molecule (ICAM)-1 concentration before (V1) and during therapy (V4), and at 3 (V5) and 6 months (V6) after the last IVIg injection. The ICAM-1 concentration was significantly lower at the 3-month follow-up visit (V5) compared with the concentration at V1, but it had increased by the 6-month follow-up visit (V6).
Figure Legend Snippet: Intracellular cell adhesion molecule (ICAM)-1 concentration before (V1) and during therapy (V4), and at 3 (V5) and 6 months (V6) after the last IVIg injection. The ICAM-1 concentration was significantly lower at the 3-month follow-up visit (V5) compared with the concentration at V1, but it had increased by the 6-month follow-up visit (V6).

Techniques Used: Concentration Assay, Injection

13) Product Images from "Pseudomonas aeruginosa Suppresses Interferon Response to Rhinovirus Infection in Cystic Fibrosis but Not in Normal Bronchial Epithelial Cells ▿ Suppresses Interferon Response to Rhinovirus Infection in Cystic Fibrosis but Not in Normal Bronchial Epithelial Cells ▿ §"

Article Title: Pseudomonas aeruginosa Suppresses Interferon Response to Rhinovirus Infection in Cystic Fibrosis but Not in Normal Bronchial Epithelial Cells ▿ Suppresses Interferon Response to Rhinovirus Infection in Cystic Fibrosis but Not in Normal Bronchial Epithelial Cells ▿ §

Journal: Infection and Immunity

doi: 10.1128/IAI.05120-11

MPA infection increases ICAM-1 expression and binding of RV to bronchial epithelial cells. IB3 (A) or BEAS-2B (B) cells were infected with MPA and immunostained with antibody to ICAM-1 and analyzed by flow cytometry. Representative histogram (A and B) and mean fluorescence intensity (C) from three independent experiments. MPA-infected cells were incubated with RV39 or the same volume of sham in the presence or absence of 10 mM EDTA for 1 h at 4°C. Cells were washed and immunolabeled with antibody to RV and subjected to flow cytometry. Specific binding was calculated by subtracting the MFI associated with cells incubated with sham, as well as the MFI obtained in the presence of EDTA, from the MFI obtained in the absence of EDTA (D). To determine endocytosis of RV, cells were incubated with virus, unbound virus was removed, and cells were shifted to 33°C and incubated for another 30 min. Cells were washed and immunolabeled, and the MFI determined as described above (E). Data in panels C, D, and E represent averages ± SD calculated from four independent experiments performed in duplicate. *, different from sham-treated group ( P ≤ 0.05) (Student's t test). FITC, fluorescein isothiocyanate.
Figure Legend Snippet: MPA infection increases ICAM-1 expression and binding of RV to bronchial epithelial cells. IB3 (A) or BEAS-2B (B) cells were infected with MPA and immunostained with antibody to ICAM-1 and analyzed by flow cytometry. Representative histogram (A and B) and mean fluorescence intensity (C) from three independent experiments. MPA-infected cells were incubated with RV39 or the same volume of sham in the presence or absence of 10 mM EDTA for 1 h at 4°C. Cells were washed and immunolabeled with antibody to RV and subjected to flow cytometry. Specific binding was calculated by subtracting the MFI associated with cells incubated with sham, as well as the MFI obtained in the presence of EDTA, from the MFI obtained in the absence of EDTA (D). To determine endocytosis of RV, cells were incubated with virus, unbound virus was removed, and cells were shifted to 33°C and incubated for another 30 min. Cells were washed and immunolabeled, and the MFI determined as described above (E). Data in panels C, D, and E represent averages ± SD calculated from four independent experiments performed in duplicate. *, different from sham-treated group ( P ≤ 0.05) (Student's t test). FITC, fluorescein isothiocyanate.

Techniques Used: Infection, Expressing, Binding Assay, Flow Cytometry, Cytometry, Fluorescence, Incubation, Immunolabeling

14) Product Images from "The Effects of Subacute Inhaled Multi-Walled Carbon Nanotube Exposure on Signaling Pathways Associated with Cholesterol Transport and Inflammatory Markers in the Vasculature of Wild-Type Mice."

Article Title: The Effects of Subacute Inhaled Multi-Walled Carbon Nanotube Exposure on Signaling Pathways Associated with Cholesterol Transport and Inflammatory Markers in the Vasculature of Wild-Type Mice.

Journal: Toxicology letters

doi: 10.1016/j.toxlet.2018.08.004

Expression of biomarkers of coronary artery disease in MWCNT vs. filtered-air exposed C57Bl/6 mice. RT-qPCR analysis of (A) ICAM-1 mRNA; (B) VCAM-1 mRNA; (C) ET-1 mRNA; (D) TNF-α mRNA; (E) IL-16 mRNA; and (F) IL-1β mRNA expression between filtered air (FA)-CT and MWCNT-exposed mice. Data reported as mean normalized gene expression to GAPDH reference gene. An n=7 per group was used to analyze each gene of interest. *p
Figure Legend Snippet: Expression of biomarkers of coronary artery disease in MWCNT vs. filtered-air exposed C57Bl/6 mice. RT-qPCR analysis of (A) ICAM-1 mRNA; (B) VCAM-1 mRNA; (C) ET-1 mRNA; (D) TNF-α mRNA; (E) IL-16 mRNA; and (F) IL-1β mRNA expression between filtered air (FA)-CT and MWCNT-exposed mice. Data reported as mean normalized gene expression to GAPDH reference gene. An n=7 per group was used to analyze each gene of interest. *p

Techniques Used: Expressing, Mouse Assay, Quantitative RT-PCR

15) Product Images from "Hepatocyte Growth Factor preferentially activates the anti-inflammatory arm of NF-?B signaling to induce A20 and protect renal proximal tubular epithelial cells from inflammation"

Article Title: Hepatocyte Growth Factor preferentially activates the anti-inflammatory arm of NF-?B signaling to induce A20 and protect renal proximal tubular epithelial cells from inflammation

Journal: Journal of Cellular Physiology

doi: 10.1002/jcp.22851

HGF does not upregulate pro-inflammatory cell surface adhesion molecules ICAM-1 and VCAM-1 and chemokine MCP-1 in RPTEC
Figure Legend Snippet: HGF does not upregulate pro-inflammatory cell surface adhesion molecules ICAM-1 and VCAM-1 and chemokine MCP-1 in RPTEC

Techniques Used:

16) Product Images from "RIPK3-MLKL-mediated necroinflammation contributes to AKI progression to CKD"

Article Title: RIPK3-MLKL-mediated necroinflammation contributes to AKI progression to CKD

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0936-8

Ripk3 −/− and Mlkl −/− mice displayed reduced tubulointerstitial inflammation post IRI. All mice were subjected to IRI with 40-min ischemia. a , f Representative images of immunohistochemistry of kidney tissues with the monocytes-macrophage marker F4/80 + at 2, 14 days and 1, 3 months following IRI. Bar = 100 μM. b , g The number of F4/80-positive cells per hpf was quantified. Quantitative RT-PCR ( c , d , h – j ) and western blot analysis for RIPK3, MLKL ICAM-1 and MCP-1 ( e , k ) of the freshly isolated renal tubules from mice on 2 days and 7 days after IRI. n = 6. ** P
Figure Legend Snippet: Ripk3 −/− and Mlkl −/− mice displayed reduced tubulointerstitial inflammation post IRI. All mice were subjected to IRI with 40-min ischemia. a , f Representative images of immunohistochemistry of kidney tissues with the monocytes-macrophage marker F4/80 + at 2, 14 days and 1, 3 months following IRI. Bar = 100 μM. b , g The number of F4/80-positive cells per hpf was quantified. Quantitative RT-PCR ( c , d , h – j ) and western blot analysis for RIPK3, MLKL ICAM-1 and MCP-1 ( e , k ) of the freshly isolated renal tubules from mice on 2 days and 7 days after IRI. n = 6. ** P

Techniques Used: Mouse Assay, Immunohistochemistry, Marker, Quantitative RT-PCR, Western Blot, Isolation

17) Product Images from "Obesity-induced adipokine imbalance impairs mouse pulmonary vascular endothelial function and primes the lung for injury"

Article Title: Obesity-induced adipokine imbalance impairs mouse pulmonary vascular endothelial function and primes the lung for injury

Journal: Scientific Reports

doi: 10.1038/srep11362

Obesity impairs endothelial junction and leads to vascular injury. ( a ) Transcript levels for ICAM-1, VCAM-1 and E-selectin in the lungs of lean and obese mice at 24 h after LPS administration (n = 4, *p
Figure Legend Snippet: Obesity impairs endothelial junction and leads to vascular injury. ( a ) Transcript levels for ICAM-1, VCAM-1 and E-selectin in the lungs of lean and obese mice at 24 h after LPS administration (n = 4, *p

Techniques Used: Mouse Assay

18) Product Images from "Mycoplasma suis infection results endothelial cell damage and activation: new insight into the cell tropism and pathogenicity of hemotrophic mycoplasma"

Article Title: Mycoplasma suis infection results endothelial cell damage and activation: new insight into the cell tropism and pathogenicity of hemotrophic mycoplasma

Journal: Veterinary Research

doi: 10.1186/1297-9716-44-6

CAM expression in M. suis infected endothelial cells. The expression profiles of adhesion molecules on endothelial cells were analyzed using a FACSCanto II cell sorting system. A . Dashed lines represent the isotype control; solid lines represent cells incubated with the negative control preparation; grey histograms represent PEDSV.15 cells incubated with M. suis (1 × 10 4 cells/mL). B . Percent increase in expression ICAM-1 (CD54), PECAM-1 (CD31), E (CD62E)- and P (CD62P)-selectin in ECs infected with M. suis .
Figure Legend Snippet: CAM expression in M. suis infected endothelial cells. The expression profiles of adhesion molecules on endothelial cells were analyzed using a FACSCanto II cell sorting system. A . Dashed lines represent the isotype control; solid lines represent cells incubated with the negative control preparation; grey histograms represent PEDSV.15 cells incubated with M. suis (1 × 10 4 cells/mL). B . Percent increase in expression ICAM-1 (CD54), PECAM-1 (CD31), E (CD62E)- and P (CD62P)-selectin in ECs infected with M. suis .

Techniques Used: Chick Chorioallantoic Membrane Assay, Expressing, Infection, FACS, Incubation, Negative Control

19) Product Images from "Plasmodium falciparum Uses gC1qR/HABP1/p32 as a Receptor to Bind to Vascular Endothelium and for Platelet-Mediated Clumping"

Article Title: Plasmodium falciparum Uses gC1qR/HABP1/p32 as a Receptor to Bind to Vascular Endothelium and for Platelet-Mediated Clumping

Journal: PLoS Pathogens

doi: 10.1371/journal.ppat.0030130

Inhibition of IRBCs Binding to HUVECs with Soluble gC1qR/HABP1 and Mouse Antiserum against gC1qR/HABP1 Binding of IRBCs to HUVECs in the presence of soluble proteins is expressed as relative binding compared to binding in absence of any protein (No protein). Binding in the presence of serum is expressed as relative binding compared to binding in absence of any serum (No sera). Recombinant gC1qR/HABP1 inhibits binding of IGH-CR14+ (A) and 3D7+ (C) to HUVECs in a dose-dependent manner. Recombinant ICAM-1-Fc and BSA have no effect on binding of IGH-CR14+ (A) and 3D7+ (C) to HUVECs. Anti-gC1qR/HABP1 mouse serum inhibits binding of IGH-CR14+ (B) and 3D7+ (D) to HUVECs. Pre-immune mouse serum (PIS), anti-ICAM-1 monoclonal antibody 15.2, and anti-CD36 monoclonal antibody SMΦ do not have any effect on binding of IGH-CR14+ (B) and 3D7+ (D) to HUVECs. The number of IRBCs bound per 100 HUVECs was scored in each assay. All data are averages (± standard error) derived from two independent experiments. Each assay was performed in duplicate. Binding of IGH-CR14+ and 3D7+ IRBCs in absence of any protein or serum was in the range of 150–200 IRBCs bound to 100 HUVECs.
Figure Legend Snippet: Inhibition of IRBCs Binding to HUVECs with Soluble gC1qR/HABP1 and Mouse Antiserum against gC1qR/HABP1 Binding of IRBCs to HUVECs in the presence of soluble proteins is expressed as relative binding compared to binding in absence of any protein (No protein). Binding in the presence of serum is expressed as relative binding compared to binding in absence of any serum (No sera). Recombinant gC1qR/HABP1 inhibits binding of IGH-CR14+ (A) and 3D7+ (C) to HUVECs in a dose-dependent manner. Recombinant ICAM-1-Fc and BSA have no effect on binding of IGH-CR14+ (A) and 3D7+ (C) to HUVECs. Anti-gC1qR/HABP1 mouse serum inhibits binding of IGH-CR14+ (B) and 3D7+ (D) to HUVECs. Pre-immune mouse serum (PIS), anti-ICAM-1 monoclonal antibody 15.2, and anti-CD36 monoclonal antibody SMΦ do not have any effect on binding of IGH-CR14+ (B) and 3D7+ (D) to HUVECs. The number of IRBCs bound per 100 HUVECs was scored in each assay. All data are averages (± standard error) derived from two independent experiments. Each assay was performed in duplicate. Binding of IGH-CR14+ and 3D7+ IRBCs in absence of any protein or serum was in the range of 150–200 IRBCs bound to 100 HUVECs.

Techniques Used: Inhibition, Binding Assay, Protein Binding, Recombinant, Derivative Assay

Inhibition of IRBCs Binding to HBMECs with Soluble gC1qR/HABP1 and Mouse Antiserum against gC1qR/HABP1 Binding of IRBCs to HBMECs in the presence of soluble proteins is expressed as relative binding compared to binding in absence of any protein (No protein). Binding in the presence of serum is expressed as relative binding compared to binding in absence of any serum (No serum). Recombinant gC1qR/HABP1 inhibits binding of IGH-CR14+ (A) to HBMECs in a dose-dependent manner. Recombinant ICAM-1-Fc, CD36-Fc, and BSA have no effect on binding of IGH-CR14+ (A). Anti-gC1qR/HABP1 mouse serum inhibits binding of IGH-CR14+ (B) to HBMECs. Pre-immune mouse serum (PIS), anti-ICAM-1 monoclonal antibody (clone 15.2), and anti-CD36 monoclonal antibody (clone SMΦ) do not have any effect on binding of IGH-CR14+ (B) to HBMECs. The number of IRBCs bound to 100 HBMEC cells was scored in each assay. All data are averages (± standard error) derived from two independent experiments. Each assay was performed in duplicate. Binding of IGH-CR14+ in absence of any protein or serum was in the range of 90–100 IRBCs bound to 100 HBMECs.
Figure Legend Snippet: Inhibition of IRBCs Binding to HBMECs with Soluble gC1qR/HABP1 and Mouse Antiserum against gC1qR/HABP1 Binding of IRBCs to HBMECs in the presence of soluble proteins is expressed as relative binding compared to binding in absence of any protein (No protein). Binding in the presence of serum is expressed as relative binding compared to binding in absence of any serum (No serum). Recombinant gC1qR/HABP1 inhibits binding of IGH-CR14+ (A) to HBMECs in a dose-dependent manner. Recombinant ICAM-1-Fc, CD36-Fc, and BSA have no effect on binding of IGH-CR14+ (A). Anti-gC1qR/HABP1 mouse serum inhibits binding of IGH-CR14+ (B) to HBMECs. Pre-immune mouse serum (PIS), anti-ICAM-1 monoclonal antibody (clone 15.2), and anti-CD36 monoclonal antibody (clone SMΦ) do not have any effect on binding of IGH-CR14+ (B) to HBMECs. The number of IRBCs bound to 100 HBMEC cells was scored in each assay. All data are averages (± standard error) derived from two independent experiments. Each assay was performed in duplicate. Binding of IGH-CR14+ in absence of any protein or serum was in the range of 90–100 IRBCs bound to 100 HBMECs.

Techniques Used: Inhibition, Binding Assay, Protein Binding, Recombinant, Derivative Assay

20) Product Images from "C1q Deficiency Promotes Pulmonary Vascular Inflammation and Enhances the Susceptibility of the Lung Endothelium to Injury *"

Article Title: C1q Deficiency Promotes Pulmonary Vascular Inflammation and Enhances the Susceptibility of the Lung Endothelium to Injury *

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M115.690784

C1q deficiency enhances lung endothelial cell activation. A , transcript levels for ICAM-1, VCAM-1, and E-selectin in the lungs of C1q −/− and wild type mice ( n = 4, *, p
Figure Legend Snippet: C1q deficiency enhances lung endothelial cell activation. A , transcript levels for ICAM-1, VCAM-1, and E-selectin in the lungs of C1q −/− and wild type mice ( n = 4, *, p

Techniques Used: Activation Assay, Mouse Assay

C1q deficiency aggravates LPS and acid-induced activation of lung endothelium. A , transcript levels for ICAM-1, VCAM-1 and E-selectin in the lungs of C1q −/− and wild type mice ( n = 4; *, p
Figure Legend Snippet: C1q deficiency aggravates LPS and acid-induced activation of lung endothelium. A , transcript levels for ICAM-1, VCAM-1 and E-selectin in the lungs of C1q −/− and wild type mice ( n = 4; *, p

Techniques Used: Activation Assay, Mouse Assay

21) Product Images from "Mechanical induction of group V phospholipase A2 causes lung inflammation and acute lung injury"

Article Title: Mechanical induction of group V phospholipase A2 causes lung inflammation and acute lung injury

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

doi: 10.1152/ajplung.00047.2013

Involvement of ICAM-1 in CS-induced EC-PMN adhesion and gVPLA2 upregulation. A : human pulmonary EC were exposed to 18% CS (4 h) with or without addition of ICAM-1 blocking antibody (25 μg/ml), and PMN adhesion assay at the end of CS experiment
Figure Legend Snippet: Involvement of ICAM-1 in CS-induced EC-PMN adhesion and gVPLA2 upregulation. A : human pulmonary EC were exposed to 18% CS (4 h) with or without addition of ICAM-1 blocking antibody (25 μg/ml), and PMN adhesion assay at the end of CS experiment

Techniques Used: Blocking Assay, Cell Adhesion Assay

Role of gVPLA2 in stretch-induced intercellular adhesion molecule (ICAM)-1 expression by pulmonary EC. A : human pulmonary EC were exposed to 18% CS (4 and 24 h), and ICAM-1 surface expression was evaluated by FACS scan analysis as described in materials
Figure Legend Snippet: Role of gVPLA2 in stretch-induced intercellular adhesion molecule (ICAM)-1 expression by pulmonary EC. A : human pulmonary EC were exposed to 18% CS (4 and 24 h), and ICAM-1 surface expression was evaluated by FACS scan analysis as described in materials

Techniques Used: Expressing, FACS

22) Product Images from "Plasmodium Falciparum Intercellular Adhesion Molecule-1-Based Cytoadherence-Related Signaling in Human Endothelial Cells"

Article Title: Plasmodium Falciparum Intercellular Adhesion Molecule-1-Based Cytoadherence-Related Signaling in Human Endothelial Cells

Journal:

doi: 10.1086/518795

Signaling activities by human umbilical vein endothelial cells (HUVECs) as a ratio of intercellular adhesion molecule (ICAM)-1 cross-linking caused by different parasite lines (C24, ItG, and A4) and red blood cells (RBCs) in the absence and presence of
Figure Legend Snippet: Signaling activities by human umbilical vein endothelial cells (HUVECs) as a ratio of intercellular adhesion molecule (ICAM)-1 cross-linking caused by different parasite lines (C24, ItG, and A4) and red blood cells (RBCs) in the absence and presence of

Techniques Used:

Differential effect of binding to human umbilical vein endothelial cells (intercellular adhesion molecule [ICAM]-1 Kilifi homozygous, heterozygous, and reference [ref] genotypes) with Plasmodium falciparum lines ItG, A4, and C24. hp, high power.
Figure Legend Snippet: Differential effect of binding to human umbilical vein endothelial cells (intercellular adhesion molecule [ICAM]-1 Kilifi homozygous, heterozygous, and reference [ref] genotypes) with Plasmodium falciparum lines ItG, A4, and C24. hp, high power.

Techniques Used: Binding Assay

Signaling activities by human dermal microvascular endothelial cells as a ratio of intercellular adhesion molecule (ICAM)-1 cross-linking caused by different parasite lines (C24 and ItG) and mock-incubated uninfected red blood cells (RBCs) in the absence
Figure Legend Snippet: Signaling activities by human dermal microvascular endothelial cells as a ratio of intercellular adhesion molecule (ICAM)-1 cross-linking caused by different parasite lines (C24 and ItG) and mock-incubated uninfected red blood cells (RBCs) in the absence

Techniques Used: Incubation

23) Product Images from "The proadhesive phenotype of systemic sclerosis skin promotes myeloid cell adhesion via ICAM-1 and VCAM-1"

Article Title: The proadhesive phenotype of systemic sclerosis skin promotes myeloid cell adhesion via ICAM-1 and VCAM-1

Journal: Rheumatology (Oxford, England)

doi: 10.1093/rheumatology/kep091

The expression of VCAM-1 and ICAM-1 on SSc dermal fibroblasts is highly inducible. Cell surface ELISAs were performed to determine if VCAM-1 and ICAM-1 expression on the surface of SSc dermal fibroblasts was inducible by cytokine stimulation. ( A ) VCAM-1
Figure Legend Snippet: The expression of VCAM-1 and ICAM-1 on SSc dermal fibroblasts is highly inducible. Cell surface ELISAs were performed to determine if VCAM-1 and ICAM-1 expression on the surface of SSc dermal fibroblasts was inducible by cytokine stimulation. ( A ) VCAM-1

Techniques Used: Expressing

ICAM-1 and VCAM-1 mediate adhesion of U937 cells to proximal and distal SSc skin. Stamper–Woodruff in situ assays were performed using frozen skin sections and fluorescent-labelled U937 cells. The percent of maximal binding was defined as the
Figure Legend Snippet: ICAM-1 and VCAM-1 mediate adhesion of U937 cells to proximal and distal SSc skin. Stamper–Woodruff in situ assays were performed using frozen skin sections and fluorescent-labelled U937 cells. The percent of maximal binding was defined as the

Techniques Used: In Situ, Binding Assay

ICAM-1 mediates adhesion of U937 cells to SSc dermal fibroblasts. Adhesion assays were performed using U937 cells and SSc dermal fibroblasts in the presence of neutralizing antibodies against ICAM-1 ( A ), CD99 ( B ), JAM-B ( C ) and JAM-C ( D ). The percent
Figure Legend Snippet: ICAM-1 mediates adhesion of U937 cells to SSc dermal fibroblasts. Adhesion assays were performed using U937 cells and SSc dermal fibroblasts in the presence of neutralizing antibodies against ICAM-1 ( A ), CD99 ( B ), JAM-B ( C ) and JAM-C ( D ). The percent

Techniques Used:

24) Product Images from "Chemokines, chemokine receptors and adhesion molecules on different human endothelia: discriminating the tissue-specific functions that affect leucocyte migration"

Article Title: Chemokines, chemokine receptors and adhesion molecules on different human endothelia: discriminating the tissue-specific functions that affect leucocyte migration

Journal: Clinical and Experimental Immunology

doi: 10.1111/j.1365-2249.2003.02323.x

Individual variation in adhesion molecule expression. Surface expression of ICAM-1, ICAM-2, VCAM, E-selectin and MHC class I (positive control) was measured by ELISA on endothelium from three different SVEC donors run in parallel. The cells were either unstimulated (control) or stimulated by TNF- α , or IFN- γ or both cytokines together for 24 h. Values shown are the mean ± s.d. of three replicate determinations.
Figure Legend Snippet: Individual variation in adhesion molecule expression. Surface expression of ICAM-1, ICAM-2, VCAM, E-selectin and MHC class I (positive control) was measured by ELISA on endothelium from three different SVEC donors run in parallel. The cells were either unstimulated (control) or stimulated by TNF- α , or IFN- γ or both cytokines together for 24 h. Values shown are the mean ± s.d. of three replicate determinations.

Techniques Used: Expressing, Positive Control, Enzyme-linked Immunosorbent Assay

Expression of adhesion molecules on different endothelia. Surface expression of ICAM-1, ICAM-2, VCAM, PECAM, E/P-selectin and MHC class I (positive control) was measured by ELISA on endothelium from five different tissues. The bars for the endothelia are from left to right: BMEC (black), SVEC, DMVEC, LMVEC and HUVEC (white). Values shown are the mean ± s.d. of three replicate determinations.
Figure Legend Snippet: Expression of adhesion molecules on different endothelia. Surface expression of ICAM-1, ICAM-2, VCAM, PECAM, E/P-selectin and MHC class I (positive control) was measured by ELISA on endothelium from five different tissues. The bars for the endothelia are from left to right: BMEC (black), SVEC, DMVEC, LMVEC and HUVEC (white). Values shown are the mean ± s.d. of three replicate determinations.

Techniques Used: Expressing, Positive Control, Enzyme-linked Immunosorbent Assay

25) Product Images from "The role of the lectin-like oxLDL receptor (LOX-1) in traffic-generated air pollution exposure-mediated alteration of the brain microvasculature in Apolipoprotein (Apo) E knockout mice"

Article Title: The role of the lectin-like oxLDL receptor (LOX-1) in traffic-generated air pollution exposure-mediated alteration of the brain microvasculature in Apolipoprotein (Apo) E knockout mice

Journal: Inhalation toxicology

doi: 10.1080/08958378.2017.1357774

MVE-exposure mediates increased expression of adhesion and cytokine molecules, which is mediated via LOX-1 receptor signaling. RT-qPCR analysis of in the cerebral microvessels of (A) intracellular adhesion molecule (ICAM)-1; (B) vascular cell adhesion molecule (VCAM)-1; and (C) monocyte chemoattractant protein (MCP)-1 in ApoE −/− mice exposed to either filtered air (FA)+ IgG; FA + LOX-1 Ab (16 mg/ml, 0.1 ml/mouse, every other day throughout exposure); 100 PM μg/m 3 of mixed vehicular emission (MVE) + IgG; or MVE + LOX-1 Ab for 6 h/d, 7 d/week, for 30 d. * p
Figure Legend Snippet: MVE-exposure mediates increased expression of adhesion and cytokine molecules, which is mediated via LOX-1 receptor signaling. RT-qPCR analysis of in the cerebral microvessels of (A) intracellular adhesion molecule (ICAM)-1; (B) vascular cell adhesion molecule (VCAM)-1; and (C) monocyte chemoattractant protein (MCP)-1 in ApoE −/− mice exposed to either filtered air (FA)+ IgG; FA + LOX-1 Ab (16 mg/ml, 0.1 ml/mouse, every other day throughout exposure); 100 PM μg/m 3 of mixed vehicular emission (MVE) + IgG; or MVE + LOX-1 Ab for 6 h/d, 7 d/week, for 30 d. * p

Techniques Used: Expressing, Quantitative RT-PCR, Mouse Assay

26) Product Images from "RIPK3-MLKL-mediated necroinflammation contributes to AKI progression to CKD"

Article Title: RIPK3-MLKL-mediated necroinflammation contributes to AKI progression to CKD

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0936-8

Ripk3 −/− and Mlkl −/− mice displayed reduced tubulointerstitial inflammation post IRI. All mice were subjected to IRI with 40-min ischemia. a , f Representative images of immunohistochemistry of kidney tissues with the monocytes-macrophage marker F4/80 + at 2, 14 days and 1, 3 months following IRI. Bar = 100 μM. b , g The number of F4/80-positive cells per hpf was quantified. Quantitative RT-PCR ( c , d , h – j ) and western blot analysis for RIPK3, MLKL ICAM-1 and MCP-1 ( e , k ) of the freshly isolated renal tubules from mice on 2 days and 7 days after IRI. n = 6. ** P
Figure Legend Snippet: Ripk3 −/− and Mlkl −/− mice displayed reduced tubulointerstitial inflammation post IRI. All mice were subjected to IRI with 40-min ischemia. a , f Representative images of immunohistochemistry of kidney tissues with the monocytes-macrophage marker F4/80 + at 2, 14 days and 1, 3 months following IRI. Bar = 100 μM. b , g The number of F4/80-positive cells per hpf was quantified. Quantitative RT-PCR ( c , d , h – j ) and western blot analysis for RIPK3, MLKL ICAM-1 and MCP-1 ( e , k ) of the freshly isolated renal tubules from mice on 2 days and 7 days after IRI. n = 6. ** P

Techniques Used: Mouse Assay, Immunohistochemistry, Marker, Quantitative RT-PCR, Western Blot, Isolation

27) Product Images from "Proinflammatory Cytokine, Chemokine, and Cellular Adhesion Molecule Expression during the Acute Phase of Experimental Brain Abscess Development"

Article Title: Proinflammatory Cytokine, Chemokine, and Cellular Adhesion Molecule Expression during the Acute Phase of Experimental Brain Abscess Development

Journal: The American Journal of Pathology

doi:

Expression of both PECAM and ICAM-1 is up-regulated on vascular endothelium in early brain abscess lesions. Adult Lewis rats were implanted with S. aureus -containing or sterile beads. Brain sections from animals perfusion-fixed with 4% paraformaldehyde/0.1 mol/L phosphate buffer were stained with antibodies specific for PECAM or ICAM-1 or an isotype-matched control antibody for immunohistochemical analysis. Images shown represent tissues collected at 48 hours after implantation of S. aureus or sterile beads. Arrows delineate vascular endothelium expressing PECAM or ICAM-1. Original magnification, ×100.
Figure Legend Snippet: Expression of both PECAM and ICAM-1 is up-regulated on vascular endothelium in early brain abscess lesions. Adult Lewis rats were implanted with S. aureus -containing or sterile beads. Brain sections from animals perfusion-fixed with 4% paraformaldehyde/0.1 mol/L phosphate buffer were stained with antibodies specific for PECAM or ICAM-1 or an isotype-matched control antibody for immunohistochemical analysis. Images shown represent tissues collected at 48 hours after implantation of S. aureus or sterile beads. Arrows delineate vascular endothelium expressing PECAM or ICAM-1. Original magnification, ×100.

Techniques Used: Expressing, Staining, Immunohistochemistry

28) Product Images from "Heme oxygenase-1 is a modulator of inflammation and vaso-occlusion in transgenic sickle mice"

Article Title: Heme oxygenase-1 is a modulator of inflammation and vaso-occlusion in transgenic sickle mice

Journal:

doi: 10.1172/JCI26857

Further upregulation of HO-1 by hemin inhibits NF-κB activation and VCAM-1 and ICAM-1 overexpression in the organs of sickle mice. S+S-Antilles mice were either untreated or injected with hemin (40 μmol/kg/d, i.p.) for 3 days.
Figure Legend Snippet: Further upregulation of HO-1 by hemin inhibits NF-κB activation and VCAM-1 and ICAM-1 overexpression in the organs of sickle mice. S+S-Antilles mice were either untreated or injected with hemin (40 μmol/kg/d, i.p.) for 3 days.

Techniques Used: Activation Assay, Over Expression, Mouse Assay, Injection

29) Product Images from "Enterovirus Capsid Interactions with Decay-Accelerating Factor Mediate Lytic Cell Infection"

Article Title: Enterovirus Capsid Interactions with Decay-Accelerating Factor Mediate Lytic Cell Infection

Journal: Journal of Virology

doi: 10.1128/JVI.78.3.1431-1439.2004

Binding of [ 35 S]methionine-labeled CVA21 prototype Kuykendall (A) and clinical isolate 272101 (B) to HeLa cells in the presence of an anti-DAF SCR 1 MAb, an anti-ICAM-1 domain 1 MAb, and/or PI-PLC treatment. The levels of [ 35 S]methionine-labeled virus bound were determined by liquid scintillation counting. The results are expressed as the means of triplicate samples plus the SD.
Figure Legend Snippet: Binding of [ 35 S]methionine-labeled CVA21 prototype Kuykendall (A) and clinical isolate 272101 (B) to HeLa cells in the presence of an anti-DAF SCR 1 MAb, an anti-ICAM-1 domain 1 MAb, and/or PI-PLC treatment. The levels of [ 35 S]methionine-labeled virus bound were determined by liquid scintillation counting. The results are expressed as the means of triplicate samples plus the SD.

Techniques Used: Binding Assay, Labeling, Planar Chromatography

Binding of [ 35 S]methionine-labeled CVA21 prototype (Kuykendall) and three CVA21 clinical isolates (272101, 275238, and 272598) to DAF-expressing CHO cells (A) and ICAM-1-expressing CHO cells (B) in the presence or absence of an anti-ICAM-1 MAb. The levels of [ 35 S]methionine-labeled virus bound were determined by liquid scintillation counting. The results are expressed as the means of triplicate samples plus the SD.
Figure Legend Snippet: Binding of [ 35 S]methionine-labeled CVA21 prototype (Kuykendall) and three CVA21 clinical isolates (272101, 275238, and 272598) to DAF-expressing CHO cells (A) and ICAM-1-expressing CHO cells (B) in the presence or absence of an anti-ICAM-1 MAb. The levels of [ 35 S]methionine-labeled virus bound were determined by liquid scintillation counting. The results are expressed as the means of triplicate samples plus the SD.

Techniques Used: Binding Assay, Labeling, Expressing

Lytic infection of ICAM-1-negative RD cells by the CVA21 prototype (Kuykendall) and clinical isolates (272101, 275238, and 272598) in the presence of anti-DAF MAbs IA10 (SCR 1), VIIIA7 (SCR 2), IH4 (SCR 3), and IIH6 (SCR 4). Anti-DAF MAbs (20 μg/ml) were added to monolayers of RD cells cultured in 96-well plates. After incubation for 1 h at 37°C, the cells were challenged with ∼10 3 50% tissue culture infective dose(s) of the CVA21 isolates/well and incubated for 48 h at 37°C. Cell lysis was assessed by staining the cell monolayers with a crystal violet-methanol solution and then measuring the absorbance at 540 nm. The results are expressed as the mean percentage lysis of duplicate wells.
Figure Legend Snippet: Lytic infection of ICAM-1-negative RD cells by the CVA21 prototype (Kuykendall) and clinical isolates (272101, 275238, and 272598) in the presence of anti-DAF MAbs IA10 (SCR 1), VIIIA7 (SCR 2), IH4 (SCR 3), and IIH6 (SCR 4). Anti-DAF MAbs (20 μg/ml) were added to monolayers of RD cells cultured in 96-well plates. After incubation for 1 h at 37°C, the cells were challenged with ∼10 3 50% tissue culture infective dose(s) of the CVA21 isolates/well and incubated for 48 h at 37°C. Cell lysis was assessed by staining the cell monolayers with a crystal violet-methanol solution and then measuring the absorbance at 540 nm. The results are expressed as the mean percentage lysis of duplicate wells.

Techniques Used: Infection, Cell Culture, Incubation, Lysis, Staining

Binding of [ 35 S]methionine-labeled CVA21 prototype (Kuykendall) and three CVA21 clinical isolates (272101, 275238, and 272598) to CHO cells expressing either DAF or ICAM-1 alone or in combination. (A) Flow cytometric analysis of surface DAF and ICAM-1 expression. Transfected CHO cells were incubated with either conjugate alone, anti-DAF MAb (IH4), or anti-ICAM-1 MAb (WEHI), and the specific binding was measured on a FACStar analyzer. The filled histograms represent the binding of the conjugate; the solid-line histograms represent the binding of the anti-DAF MAb, and the dotted-line histograms represent the binding of the anti-ICAM-1 MAb. (B) The levels of [ 35 S]methionine-labeled virus bound were determined by liquid scintillation counting. The results are expressed as the means of triplicate samples plus the SD.
Figure Legend Snippet: Binding of [ 35 S]methionine-labeled CVA21 prototype (Kuykendall) and three CVA21 clinical isolates (272101, 275238, and 272598) to CHO cells expressing either DAF or ICAM-1 alone or in combination. (A) Flow cytometric analysis of surface DAF and ICAM-1 expression. Transfected CHO cells were incubated with either conjugate alone, anti-DAF MAb (IH4), or anti-ICAM-1 MAb (WEHI), and the specific binding was measured on a FACStar analyzer. The filled histograms represent the binding of the conjugate; the solid-line histograms represent the binding of the anti-DAF MAb, and the dotted-line histograms represent the binding of the anti-ICAM-1 MAb. (B) The levels of [ 35 S]methionine-labeled virus bound were determined by liquid scintillation counting. The results are expressed as the means of triplicate samples plus the SD.

Techniques Used: Binding Assay, Labeling, Expressing, Flow Cytometry, Transfection, Incubation

30) Product Images from "ICAM-1 and VCAM-1 antisense oligonucleotides attenuate in vivo leucocyte adherence and inflammation in rat inflammatory bowel disease"

Article Title: ICAM-1 and VCAM-1 antisense oligonucleotides attenuate in vivo leucocyte adherence and inflammation in rat inflammatory bowel disease

Journal: Gut

doi:

Adherent leucocytes 48 hours after the first application of indomethacin (Indo). The effect of antisense oligonucleotides on intestinal microcirculation observed by intravital microscopy. Two intravenous (iv) (but not subcutaneous (sc)) doses of 2 mg/kg intercellular adhesion molecule 1 (ICAM-1) antisense oligonucleotides and two iv doses of 8 mg/kg vascular cell adhesion molecule 1 (VCAM-1) antisense oligonucleotides decreased the number of adherent leucocytes significantly. Scatter plot with mean values indicated (n=10). SC, scrambled control oligonucleotides.
Figure Legend Snippet: Adherent leucocytes 48 hours after the first application of indomethacin (Indo). The effect of antisense oligonucleotides on intestinal microcirculation observed by intravital microscopy. Two intravenous (iv) (but not subcutaneous (sc)) doses of 2 mg/kg intercellular adhesion molecule 1 (ICAM-1) antisense oligonucleotides and two iv doses of 8 mg/kg vascular cell adhesion molecule 1 (VCAM-1) antisense oligonucleotides decreased the number of adherent leucocytes significantly. Scatter plot with mean values indicated (n=10). SC, scrambled control oligonucleotides.

Techniques Used: Intravital Microscopy

Rolling leucocytes 48 hours after the first application of indomethacin (Indo). The effect of antisense oligonucleotides on intestinal microcirculation observed by intravital microscopy. Two intravenous (iv) (but not subcutaneous (sc)) doses of 2 mg/kg intercellular adhesion molecule 1 (ICAM-1) antisense oligonucleotides and two iv doses of 8 mg/kg vascular cell adhesion molecule 1 (VCAM-1) antisense oligonucleotides reduced the number of rolling leucocytes significantly. Scatter plot with mean values indicated (n=10). SC, scrambled control oligonucleotides.
Figure Legend Snippet: Rolling leucocytes 48 hours after the first application of indomethacin (Indo). The effect of antisense oligonucleotides on intestinal microcirculation observed by intravital microscopy. Two intravenous (iv) (but not subcutaneous (sc)) doses of 2 mg/kg intercellular adhesion molecule 1 (ICAM-1) antisense oligonucleotides and two iv doses of 8 mg/kg vascular cell adhesion molecule 1 (VCAM-1) antisense oligonucleotides reduced the number of rolling leucocytes significantly. Scatter plot with mean values indicated (n=10). SC, scrambled control oligonucleotides.

Techniques Used: Intravital Microscopy

Histological inflammation 48 hours after the first application of indomethacin (Indo). Two intravenous (iv) (but not subcutaneous (sc)) doses of 2 mg/kg intercellular adhesion molecule 1 (ICAM-1) antisense oligonucleotides and two iv doses of 8 mg/kg vascular cell adhesion molecule 1 (VCAM-1) antisense oligonucleotides significantly diminished histological intestinal inflammation. Values are mean (SEM) (n=l 0). SC, scrambled control oligonucleotides.
Figure Legend Snippet: Histological inflammation 48 hours after the first application of indomethacin (Indo). Two intravenous (iv) (but not subcutaneous (sc)) doses of 2 mg/kg intercellular adhesion molecule 1 (ICAM-1) antisense oligonucleotides and two iv doses of 8 mg/kg vascular cell adhesion molecule 1 (VCAM-1) antisense oligonucleotides significantly diminished histological intestinal inflammation. Values are mean (SEM) (n=l 0). SC, scrambled control oligonucleotides.

Techniques Used:

Macroscopic inflammation 48 hours after the first application of indomethacin (Indo). Two intravenous (iv) (but not subcutaneous (sc)) doses of 2 mg/kg intercellular adhesion molecule 1 (ICAM-1) antisense oligonucleotides and two iv doses of both 4 mg/kg and 8 mg/kg vascular cell adhesion molecule 1 (VCAM-1) antisense oligonucleotides significantly reduced macroscopic intestinal inflammation. Values are mean (SEM) (n=l0). SC, scrambled control oligonucleotides.
Figure Legend Snippet: Macroscopic inflammation 48 hours after the first application of indomethacin (Indo). Two intravenous (iv) (but not subcutaneous (sc)) doses of 2 mg/kg intercellular adhesion molecule 1 (ICAM-1) antisense oligonucleotides and two iv doses of both 4 mg/kg and 8 mg/kg vascular cell adhesion molecule 1 (VCAM-1) antisense oligonucleotides significantly reduced macroscopic intestinal inflammation. Values are mean (SEM) (n=l0). SC, scrambled control oligonucleotides.

Techniques Used:

Intercellular adhesion molecule 1 (ICAM-1) expression in rat submucosal venules detected by immunohistochemistry using the peroxidase technique 48 hours after the first indomethacin application. (A) Frozen section of rat ileum from a healthy animal: small amounts of ICAM-1 are expressed constitutively in submucosal venules. (B) Frozen section of ileum from a rat with indomethacin induced ileitis: ICAM-1 expression is clearly upregulated in submucosal venules compared with healthy animals. (C) Frozen section of rat ileum from an animal treated with indomethacin and ICAM-1 antisense oligonucleotides at a dose of 2 mg/kg intravenously: staining of ICAM-1 in submucosal venules was markedly reduced compared with animals treated with indomethacin alone (original magnification ×200).
Figure Legend Snippet: Intercellular adhesion molecule 1 (ICAM-1) expression in rat submucosal venules detected by immunohistochemistry using the peroxidase technique 48 hours after the first indomethacin application. (A) Frozen section of rat ileum from a healthy animal: small amounts of ICAM-1 are expressed constitutively in submucosal venules. (B) Frozen section of ileum from a rat with indomethacin induced ileitis: ICAM-1 expression is clearly upregulated in submucosal venules compared with healthy animals. (C) Frozen section of rat ileum from an animal treated with indomethacin and ICAM-1 antisense oligonucleotides at a dose of 2 mg/kg intravenously: staining of ICAM-1 in submucosal venules was markedly reduced compared with animals treated with indomethacin alone (original magnification ×200).

Techniques Used: Expressing, Immunohistochemistry, Staining

31) Product Images from "Zinc modulates the innate immune response in vivo to polymicrobial sepsis through regulation of NF-?B"

Article Title: Zinc modulates the innate immune response in vivo to polymicrobial sepsis through regulation of NF-?B

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

doi: 10.1152/ajplung.00368.2009

Zinc deficiency enhances the expression of NF-κB-responsive genes in primary human lung epithelial cells. A : primary human lung epithelial cells (hLECs) were cultured onto collagen-coated, semipermeable membranes. TPEN (20 μM) or zinc (5 μM) were used to modify zinc status as previously described. Cells were then stimulated with TNFα (10 ng/ml) for 6 h to activate the NF-κB pathway. Total RNA was isolated, and the expression of NF-κB target genes was measured. B : in addition, culture supernatants were obtained and measured to determine IL-6 and ICAM-1 concentrations (total donor number: n = 3; *Zn − /CLP vs. Ctrl/CLP, P
Figure Legend Snippet: Zinc deficiency enhances the expression of NF-κB-responsive genes in primary human lung epithelial cells. A : primary human lung epithelial cells (hLECs) were cultured onto collagen-coated, semipermeable membranes. TPEN (20 μM) or zinc (5 μM) were used to modify zinc status as previously described. Cells were then stimulated with TNFα (10 ng/ml) for 6 h to activate the NF-κB pathway. Total RNA was isolated, and the expression of NF-κB target genes was measured. B : in addition, culture supernatants were obtained and measured to determine IL-6 and ICAM-1 concentrations (total donor number: n = 3; *Zn − /CLP vs. Ctrl/CLP, P

Techniques Used: Expressing, Cell Culture, Isolation

Zinc deficiency modulates NF-κB-mediated related gene expression in the lung following sepsis. C57BL/6 black mice were subjected to modified diets for 3 wk and then subjected to CLP. Mouse lungs were lavaged and perfused with saline at 24 h following CLP. Total RNA was isolated, and the expression of NF-κB-related genes was determined by real-time PCR. The genes included: the cytokines IL-1β and TNFα ( A ); NF-κB family p65, p50, IκBα, and IκB family member B cell lymphoma 3 (Bcl-3) ( B ); and chemokines CCL3 and CXCL14 and the cell adhesion molecule ICAM-1 ( C ). n = 5 lungs per treatment group; *Zn − /CLP vs. Ctrl/CLP, P
Figure Legend Snippet: Zinc deficiency modulates NF-κB-mediated related gene expression in the lung following sepsis. C57BL/6 black mice were subjected to modified diets for 3 wk and then subjected to CLP. Mouse lungs were lavaged and perfused with saline at 24 h following CLP. Total RNA was isolated, and the expression of NF-κB-related genes was determined by real-time PCR. The genes included: the cytokines IL-1β and TNFα ( A ); NF-κB family p65, p50, IκBα, and IκB family member B cell lymphoma 3 (Bcl-3) ( B ); and chemokines CCL3 and CXCL14 and the cell adhesion molecule ICAM-1 ( C ). n = 5 lungs per treatment group; *Zn − /CLP vs. Ctrl/CLP, P

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

Related Articles

Flow Cytometry:

Article Title: The sickle cell trait affects contact dynamics and endothelial cell activation in Plasmodium falciparum-infected erythrocytes
Article Snippet: .. Where indicated, cytoadhesion blocking antibodies directed against CD36 (FA6-152, Abcam) and ICAM-1 (CD54, 15.2, Serotec) were added (4 µg ml−1 in HDMEC culture media) for 1 h under regular culture conditions prior to the flow chamber experiments. .. Quantification of cytoadhesive phenotypes From the recorded fluorescence signals, two parameters were derived on a single cell basis: the fluorescence intensity and the translational velocity.

Blocking Assay:

Article Title: The sickle cell trait affects contact dynamics and endothelial cell activation in Plasmodium falciparum-infected erythrocytes
Article Snippet: .. Where indicated, cytoadhesion blocking antibodies directed against CD36 (FA6-152, Abcam) and ICAM-1 (CD54, 15.2, Serotec) were added (4 µg ml−1 in HDMEC culture media) for 1 h under regular culture conditions prior to the flow chamber experiments. .. Quantification of cytoadhesive phenotypes From the recorded fluorescence signals, two parameters were derived on a single cell basis: the fluorescence intensity and the translational velocity.

Incubation:

Article Title: Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease
Article Snippet: .. For double-staining experiments, brain sections were simultaneously incubated with 2 primary antibodies developed in different species: anti-TH (1:1,000; Peel Freez Biochemicals), anti-GFP (1:1,000; Invitrogen), anti–Glut-1 (1:300; Santa Cruz Biotechnology Inc.), anti-PCNA (1:500; Dako), anti–Mac-1 (1:250; Serotec), anti-GFAP (1:5000; Dako), anti-CD3 (1:1,000; Serotec), anti-CD8 (1:100; Serotec), anti-CD4 (1:100; Serotec), anti–ICAM-1 (1:50; Serotec), anti-albumin (1:1,000; Cappel, MP Biomedicals), and anti-p17 caspase-3 (R & D Systems). .. Sections were then incubated in specific CY3- or FITC-conjugated secondary antibodies (Jackson ImmunoResearch Laboratories Inc.) at 1:250 dilution for 90 minutes at room temperature.

Article Title: Mild Hypothermia Attenuates Intercellular Adhesion Molecule-1 Induction via Activation of Extracellular Signal-Regulated Kinase-1/2 in a Focal Cerebral Ischemia Model
Article Snippet: .. Following incubation with primary antibodies against ICAM-1 (1 : 100, Serotec), phosphorylated ERK1/2 (1 : 200, Santa Cruz), total ERK1/2 (1 : 200, Santa Cruz), STAT3 phosphorylated at Ser727 (1 : 200, Cell Signaling), and total STAT3 (1 : 200, Santa Cruz), respectively, biotin-labeled anti-IgG secondary antibody (1 : 200, Vector Labs) was treated. .. Antibodies were detected using the Vector ABC kit (Elite Vectastain ABC kit, Vector Labs) and colorized with 0.05% diaminobenzidine (DAB, Vector Labs).

Article Title: The interaction between myocardial depressant factors in endotoxemic cardiac dysfunction: role of TNF-? in TLR4-mediated ICAM-1 expression
Article Snippet: .. The membrane is subsequently incubated with a rabbit polyclonal antibody against ICAM-1 (purchased from Serotec, 1:1000 dilution with PBS containing 0.05% Tween 20 and 5% dry milk) for 60 min and with peroxidase-labeled goat anti-rabbit IgG (1:5000 dilution with PBS containing 0.05% Tween 20 and 5% dry milk) for 45 min. After a thorough wash with PBS, protein band is developed using enhanced chemiluminescence (ECL) technique. ..

Staining:

Article Title: Immunoprivileged status of the liver is controlled by Toll-like receptor 3 signaling
Article Snippet: .. Sections were stained with rat mAbs against murine MHC class I (M1/42), ICAM-1 (CD54, KAT-1; AbD Serotec), VCAM-1 (CD106, M/K-2; AbD Serotec), CD8 (53-6.7; BD Biosciences), or VL4, an mAb against the LCMV nucleoprotein. .. Sections were further stained with goat anti-CXCL9 (MIG; R & D Systems) and anti-Thy1.1 antibody (CD90.1, HIS51; BD Biosciences).

Recombinant:

Article Title: Mapping the Binding Site of a Cross-Reactive Plasmodium falciparum PfEMP1 Monoclonal Antibody Inhibitory of ICAM-1 Binding
Article Snippet: .. Specificity of adhesion to recombinant ICAM-1–Fc was determined by the preincubation of channels with 40 μg/ml anti–ICAM-1 (clone 15.2; AbD Serotec). .. SPR measurements were conducted using a BIAcore T-100 instrument (GE Healthcare).

Double Staining:

Article Title: Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease
Article Snippet: .. For double-staining experiments, brain sections were simultaneously incubated with 2 primary antibodies developed in different species: anti-TH (1:1,000; Peel Freez Biochemicals), anti-GFP (1:1,000; Invitrogen), anti–Glut-1 (1:300; Santa Cruz Biotechnology Inc.), anti-PCNA (1:500; Dako), anti–Mac-1 (1:250; Serotec), anti-GFAP (1:5000; Dako), anti-CD3 (1:1,000; Serotec), anti-CD8 (1:100; Serotec), anti-CD4 (1:100; Serotec), anti–ICAM-1 (1:50; Serotec), anti-albumin (1:1,000; Cappel, MP Biomedicals), and anti-p17 caspase-3 (R & D Systems). .. Sections were then incubated in specific CY3- or FITC-conjugated secondary antibodies (Jackson ImmunoResearch Laboratories Inc.) at 1:250 dilution for 90 minutes at room temperature.

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  • 92
    Bio-Rad intercellular adhesion molecule 1
    Regulation of inflammatory markers over prolonged culture . Fold change in mRNA expression of inflammatory genes in fibroblast-like synoviocytes (FLS), determined by real-time RT-PCR between passages 2 and 8 (P2 to P8). Expression of mRNA was measured at 16 hr for (a) IL-6, (b) chemokine ligand 2 (CCL-2), (c) vascular cell adhesion <t>molecule</t> 1 (VCAM-1) and (d) intercellular adhesion molecule 1 (ICAM-1). For each gene product data were normalized for levels of the housekeeping gene 18S rRNA and are presented as fold change in expression (± standard error) relative to the P2 control. * P
    Intercellular Adhesion Molecule 1, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 92/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Bio-Rad intercellular adhesion molecule 1 crude proteins
    GC31 suppressed lipopolysaccharide-induced intercellular adhesion <t>molecule-1</t> expression in human umbilical vein endothelial cells. The cells were treated with GC31 (0.1 μM, 1 μM, and 10 μM) or VP30 (10 μM) simultaneously combined with lipopolysaccharide (LPS) (1 μg/ml). A : The amounts of intercellular adhesion molecule-1 (ICAM-1) in the whole cell extracts 12 h after LPS stimulation were determined with western blot analysis. B : The messenger RNA (mRNA) levels of ICAM-1 were assessed with real-time PCR analysis 6 h after LPS stimulation. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein and mRNA were measured as the internal control. The data represent means±SD of triplicate measurements. *p
    Intercellular Adhesion Molecule 1 Crude Proteins, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Bio-Rad mouse anti human icam 1 antibody
    Levels of surface <t>ICAM-1</t> expression and monocyte adhesion by HMEC-1 cells after co-culture with EVs from ID2-treated placentae. Macro-, micro- and nano- vesicles were collected from first trimester human placentae that have been cultured with ID2 antibodies or isotype-matched control IgG (50 µg/mL, n = 5 placentae). Each fraction of EVs was added to confluent HMEC-1 cell monolayers for 24 hours and endothelial cell activation was quantitated by cell-based ELISA of ICAM-1 expression ( A ) or using the monocyte adhesion assay ( B ). Statistical differences were assessed by Mann-Whitney tests (*p
    Mouse Anti Human Icam 1 Antibody, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Regulation of inflammatory markers over prolonged culture . Fold change in mRNA expression of inflammatory genes in fibroblast-like synoviocytes (FLS), determined by real-time RT-PCR between passages 2 and 8 (P2 to P8). Expression of mRNA was measured at 16 hr for (a) IL-6, (b) chemokine ligand 2 (CCL-2), (c) vascular cell adhesion molecule 1 (VCAM-1) and (d) intercellular adhesion molecule 1 (ICAM-1). For each gene product data were normalized for levels of the housekeeping gene 18S rRNA and are presented as fold change in expression (± standard error) relative to the P2 control. * P

    Journal: Arthritis Research & Therapy

    Article Title: Characterisation of fibroblast-like synoviocytes from a murine model of joint inflammation

    doi: 10.1186/ar4158

    Figure Lengend Snippet: Regulation of inflammatory markers over prolonged culture . Fold change in mRNA expression of inflammatory genes in fibroblast-like synoviocytes (FLS), determined by real-time RT-PCR between passages 2 and 8 (P2 to P8). Expression of mRNA was measured at 16 hr for (a) IL-6, (b) chemokine ligand 2 (CCL-2), (c) vascular cell adhesion molecule 1 (VCAM-1) and (d) intercellular adhesion molecule 1 (ICAM-1). For each gene product data were normalized for levels of the housekeeping gene 18S rRNA and are presented as fold change in expression (± standard error) relative to the P2 control. * P

    Article Snippet: Real-time PCR Expression of mRNA for IL-6, chemokine ligand 2 (CCL-2), vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1) and bone gamma-carboxyglutamic acid-containing protein (BGLAP) was assessed using IQ SYBR Green Supermix (Bio-Rad Laboratories, Regents Park, NSW, Australia) according to the manufacturer's instructions, using a Bio-Rad iCycler iQ5 real-time PCR detection system.

    Techniques: Expressing, Quantitative RT-PCR

    Inflammatory gene regulation by corticosteone and TNF-α in FLS . Fold change in mRNA expression of inflammatory genes in (fibroblast-like synoviocytes) FLS, determined by real-time RT-PCR. Expression of mRNA was measured at 16 hr for IL-6, chemokine ligand 2 (CCL-2), vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) following pretreatment with either corticosterone (a-d) (100 nmol/l) or TNFα (e-h) (10 ng/ml) for 24 hr. Data were normalized for levels of the housekeeping gene 18S rRNA and presented as fold change in expression (± standard error) relative to untreated wild-type (WT) control FLS. * P

    Journal: Arthritis Research & Therapy

    Article Title: Characterisation of fibroblast-like synoviocytes from a murine model of joint inflammation

    doi: 10.1186/ar4158

    Figure Lengend Snippet: Inflammatory gene regulation by corticosteone and TNF-α in FLS . Fold change in mRNA expression of inflammatory genes in (fibroblast-like synoviocytes) FLS, determined by real-time RT-PCR. Expression of mRNA was measured at 16 hr for IL-6, chemokine ligand 2 (CCL-2), vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) following pretreatment with either corticosterone (a-d) (100 nmol/l) or TNFα (e-h) (10 ng/ml) for 24 hr. Data were normalized for levels of the housekeeping gene 18S rRNA and presented as fold change in expression (± standard error) relative to untreated wild-type (WT) control FLS. * P

    Article Snippet: Real-time PCR Expression of mRNA for IL-6, chemokine ligand 2 (CCL-2), vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1) and bone gamma-carboxyglutamic acid-containing protein (BGLAP) was assessed using IQ SYBR Green Supermix (Bio-Rad Laboratories, Regents Park, NSW, Australia) according to the manufacturer's instructions, using a Bio-Rad iCycler iQ5 real-time PCR detection system.

    Techniques: Expressing, Quantitative RT-PCR

    Effect of Pom on MHC-I (HLA-A, B and C), ICAM and B7-2 mRNA gene expression in BCBL-1 cells induced with butyrate BCBL-1 cells were treated with control (DMSO) or Pom (1 μM) for 24 h followed by treatment with PBS or butyrate for an additional 24 h. Total mRNA was isolated and analyzed for expression levels by real time QT-PCR and was normalized to 18S levels. Shown are the fold changes in mRNA expression for total A . HLA and HLA A, B and C alleles following treatment and B . ICAM-1 and B7-2. Values are the average +/- standard deviation of four independent experiments. *** P

    Journal: Oncotarget

    Article Title: Restoration of immune surface molecules in Kaposi sarcoma-associated herpes virus infected cells by lenalidomide and pomalidomide

    doi: 10.18632/oncotarget.17960

    Figure Lengend Snippet: Effect of Pom on MHC-I (HLA-A, B and C), ICAM and B7-2 mRNA gene expression in BCBL-1 cells induced with butyrate BCBL-1 cells were treated with control (DMSO) or Pom (1 μM) for 24 h followed by treatment with PBS or butyrate for an additional 24 h. Total mRNA was isolated and analyzed for expression levels by real time QT-PCR and was normalized to 18S levels. Shown are the fold changes in mRNA expression for total A . HLA and HLA A, B and C alleles following treatment and B . ICAM-1 and B7-2. Values are the average +/- standard deviation of four independent experiments. *** P

    Article Snippet: Primers for ICAM-1 and B7-2 were from Biorad (ICAM-1: 10025636, qHsaCED0004281) and (B7-2: 10025636, qHsaCED0043530 (Hercules, CA).

    Techniques: Expressing, Isolation, Polymerase Chain Reaction, Standard Deviation

    Restoration of ICAM-1 and B7-2 but not ICAM-3 expression in BCBL-1 cells treated with Pom A . ICAM-1 expression in BCBL-1 cells and in B . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). C . B7-2 expression in BCBL-1 cells and in D . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). E . ICAM-3 expression in BCBL-1 cells and in F . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). The data shows a representative experiment of four independent experiments for A . and C . and two independent experiments for B ., D ., and F . with similar results. The grey shading shows the isotype control.

    Journal: Oncotarget

    Article Title: Restoration of immune surface molecules in Kaposi sarcoma-associated herpes virus infected cells by lenalidomide and pomalidomide

    doi: 10.18632/oncotarget.17960

    Figure Lengend Snippet: Restoration of ICAM-1 and B7-2 but not ICAM-3 expression in BCBL-1 cells treated with Pom A . ICAM-1 expression in BCBL-1 cells and in B . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). C . B7-2 expression in BCBL-1 cells and in D . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). E . ICAM-3 expression in BCBL-1 cells and in F . BJAB cells as determined by FACS after pretreatment for 48 h with DMSO vehicle control or Pom (1 μM). The data shows a representative experiment of four independent experiments for A . and C . and two independent experiments for B ., D ., and F . with similar results. The grey shading shows the isotype control.

    Article Snippet: Primers for ICAM-1 and B7-2 were from Biorad (ICAM-1: 10025636, qHsaCED0004281) and (B7-2: 10025636, qHsaCED0043530 (Hercules, CA).

    Techniques: Expressing, FACS

    Effect of Len on ICAM-1 and B7-2 expression in BCBL-1 cells, effect of Pom on MHC-II expression in BCBL-1 and BJAB cells, and effect of Pom on ICAM-1 and B7-2 in JSC-1 cells A . ICAM-1 expression and B . B7-2 expression in BCBL-1 cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. C . ICAM-1 expression D . B7-2 expression in JSC-1 cells pretreated for 48 h with DMSO vehicle control or Pom (0.2 μM) as determined by FACS. E . MHC-II expression in BCBL-1 cells or F . BJAB cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. The data is representative of two independent experiments in A, one experiment in B-D, and two experiments in E and F. The grey shading shows the isotype control.

    Journal: Oncotarget

    Article Title: Restoration of immune surface molecules in Kaposi sarcoma-associated herpes virus infected cells by lenalidomide and pomalidomide

    doi: 10.18632/oncotarget.17960

    Figure Lengend Snippet: Effect of Len on ICAM-1 and B7-2 expression in BCBL-1 cells, effect of Pom on MHC-II expression in BCBL-1 and BJAB cells, and effect of Pom on ICAM-1 and B7-2 in JSC-1 cells A . ICAM-1 expression and B . B7-2 expression in BCBL-1 cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. C . ICAM-1 expression D . B7-2 expression in JSC-1 cells pretreated for 48 h with DMSO vehicle control or Pom (0.2 μM) as determined by FACS. E . MHC-II expression in BCBL-1 cells or F . BJAB cells pretreated for 48 h with DMSO vehicle control or Pom (1 μM) as determined by FACS. The data is representative of two independent experiments in A, one experiment in B-D, and two experiments in E and F. The grey shading shows the isotype control.

    Article Snippet: Primers for ICAM-1 and B7-2 were from Biorad (ICAM-1: 10025636, qHsaCED0004281) and (B7-2: 10025636, qHsaCED0043530 (Hercules, CA).

    Techniques: Expressing, FACS

    GC31 suppressed lipopolysaccharide-induced intercellular adhesion molecule-1 expression in human umbilical vein endothelial cells. The cells were treated with GC31 (0.1 μM, 1 μM, and 10 μM) or VP30 (10 μM) simultaneously combined with lipopolysaccharide (LPS) (1 μg/ml). A : The amounts of intercellular adhesion molecule-1 (ICAM-1) in the whole cell extracts 12 h after LPS stimulation were determined with western blot analysis. B : The messenger RNA (mRNA) levels of ICAM-1 were assessed with real-time PCR analysis 6 h after LPS stimulation. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein and mRNA were measured as the internal control. The data represent means±SD of triplicate measurements. *p

    Journal: Molecular Vision

    Article Title: Effects of a thrombomodulin-derived peptide on monocyte adhesion and intercellular adhesion molecule-1 expression in lipopolysaccharide-induced endothelial cells

    doi:

    Figure Lengend Snippet: GC31 suppressed lipopolysaccharide-induced intercellular adhesion molecule-1 expression in human umbilical vein endothelial cells. The cells were treated with GC31 (0.1 μM, 1 μM, and 10 μM) or VP30 (10 μM) simultaneously combined with lipopolysaccharide (LPS) (1 μg/ml). A : The amounts of intercellular adhesion molecule-1 (ICAM-1) in the whole cell extracts 12 h after LPS stimulation were determined with western blot analysis. B : The messenger RNA (mRNA) levels of ICAM-1 were assessed with real-time PCR analysis 6 h after LPS stimulation. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein and mRNA were measured as the internal control. The data represent means±SD of triplicate measurements. *p

    Article Snippet: Western blot analysis for intercellular adhesion molecule-1 Crude proteins were extracted from HUVECs treated with 1 μg/ml LPS in the presence or absence of GC31 (0.1–10 μM) or VP30 (10 μM) for 12 h. Protein concentration was determined using the Bio-Rad protein assay (Bio-Rad Lab).

    Techniques: Expressing, Western Blot, Real-time Polymerase Chain Reaction

    Levels of surface ICAM-1 expression and monocyte adhesion by HMEC-1 cells after co-culture with EVs from ID2-treated placentae. Macro-, micro- and nano- vesicles were collected from first trimester human placentae that have been cultured with ID2 antibodies or isotype-matched control IgG (50 µg/mL, n = 5 placentae). Each fraction of EVs was added to confluent HMEC-1 cell monolayers for 24 hours and endothelial cell activation was quantitated by cell-based ELISA of ICAM-1 expression ( A ) or using the monocyte adhesion assay ( B ). Statistical differences were assessed by Mann-Whitney tests (*p

    Journal: Scientific Reports

    Article Title: Antiphospholipid antibodies increase the levels of mitochondrial DNA in placental extracellular vesicles: Alarmin-g for preeclampsia

    doi: 10.1038/s41598-017-16448-5

    Figure Lengend Snippet: Levels of surface ICAM-1 expression and monocyte adhesion by HMEC-1 cells after co-culture with EVs from ID2-treated placentae. Macro-, micro- and nano- vesicles were collected from first trimester human placentae that have been cultured with ID2 antibodies or isotype-matched control IgG (50 µg/mL, n = 5 placentae). Each fraction of EVs was added to confluent HMEC-1 cell monolayers for 24 hours and endothelial cell activation was quantitated by cell-based ELISA of ICAM-1 expression ( A ) or using the monocyte adhesion assay ( B ). Statistical differences were assessed by Mann-Whitney tests (*p

    Article Snippet: Then, cells were washed and a mouse anti-human ICAM-1 antibody (MCA1135, Bio-rad, 1:100) was added and incubated at 37 °C for two hours, followed by a goat biotinylated anti-mouse IgG antibody (Jackson ImmunoResearch, 1:2000) and a streptavidin-conjugated HRP (Jackson ImmunoResearch, 1:2000). o-Phenylenediamine, a substrate for HRP, was added at 20 o C for detection at 490 nm using an xMark spectrophotometer (Bio-rad).

    Techniques: Expressing, Co-Culture Assay, Cell Culture, Activation Assay, In-Cell ELISA, Cell Adhesion Assay, MANN-WHITNEY

    Interactions between placental EVs and TLR-9 of HMEC-1 cells. Optical sections by fluorescence confocal microscopy showing HMEC-1 cells ( A ) that have been cultured with CellTracker TM Green CMFDA-labelled placental micro- ( B ) or nano- ( C ) vesicles (green). Lysosomes of HMEC-1 cells were labelled with LysoTracker® Red DND-99 (red) and the nuclei of HMEC-1 cells were counterstained with Hoechst (blue). Arrows show areas of co-localisation between placental EVs and lysosomes. Scale bar = 10 µm. Micro- and nano- vesicles collected from ID2-treated placentae were added to HMEC-1 cells with or without a TLR-9 antagonist (1 µM, antag, n = 6 placentae). As a positive control, HMEC-1 cells were treated with a TLR-9 agonist (5 µM). Surface ICAM-1 expression was measured by cell-based ELISA and normalised to that of untreated HMEC-1 cells ( D ). Statistical difference was assessed by Wilcoxin matched-pairs signed ranked tests (**p

    Journal: Scientific Reports

    Article Title: Antiphospholipid antibodies increase the levels of mitochondrial DNA in placental extracellular vesicles: Alarmin-g for preeclampsia

    doi: 10.1038/s41598-017-16448-5

    Figure Lengend Snippet: Interactions between placental EVs and TLR-9 of HMEC-1 cells. Optical sections by fluorescence confocal microscopy showing HMEC-1 cells ( A ) that have been cultured with CellTracker TM Green CMFDA-labelled placental micro- ( B ) or nano- ( C ) vesicles (green). Lysosomes of HMEC-1 cells were labelled with LysoTracker® Red DND-99 (red) and the nuclei of HMEC-1 cells were counterstained with Hoechst (blue). Arrows show areas of co-localisation between placental EVs and lysosomes. Scale bar = 10 µm. Micro- and nano- vesicles collected from ID2-treated placentae were added to HMEC-1 cells with or without a TLR-9 antagonist (1 µM, antag, n = 6 placentae). As a positive control, HMEC-1 cells were treated with a TLR-9 agonist (5 µM). Surface ICAM-1 expression was measured by cell-based ELISA and normalised to that of untreated HMEC-1 cells ( D ). Statistical difference was assessed by Wilcoxin matched-pairs signed ranked tests (**p

    Article Snippet: Then, cells were washed and a mouse anti-human ICAM-1 antibody (MCA1135, Bio-rad, 1:100) was added and incubated at 37 °C for two hours, followed by a goat biotinylated anti-mouse IgG antibody (Jackson ImmunoResearch, 1:2000) and a streptavidin-conjugated HRP (Jackson ImmunoResearch, 1:2000). o-Phenylenediamine, a substrate for HRP, was added at 20 o C for detection at 490 nm using an xMark spectrophotometer (Bio-rad).

    Techniques: Fluorescence, Confocal Microscopy, Cell Culture, Positive Control, Expressing, In-Cell ELISA