Structured Review

Becton Dickinson icam 1
CMH suppresses endothelial VCAM-1 and <t>ICAM-1</t> expression during EAE. a and c . Frozen sections of lumbar spinal cord taken from disease-free, EAE-normoxia or EAE-CMH mice at the peak symptomatic phase of EAE were stained for CD31 (AlexaFluor-488) and VCAM-1 (Cy-3) in panel A or CD31 (Cy-3) and ICAM-1 (AlexaFluor-488) in panel C. Scale bar = 100 μm (inset, scale bar = 50 μm). b and d . Quantification of VCAM-1 ( b ) and ICAM-1 expression ( d ). Results are expressed as the mean ± SEM ( n = 6 mice/group). Note that CMH markedly suppressed vascular expression of VCAM-1 and ICAM-1. ** p
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Images

1) Product Images from "Hypoxic pre-conditioning suppresses experimental autoimmune encephalomyelitis by modifying multiple properties of blood vessels"

Article Title: Hypoxic pre-conditioning suppresses experimental autoimmune encephalomyelitis by modifying multiple properties of blood vessels

Journal: Acta Neuropathologica Communications

doi: 10.1186/s40478-018-0590-5

CMH suppresses endothelial VCAM-1 and ICAM-1 expression during EAE. a and c . Frozen sections of lumbar spinal cord taken from disease-free, EAE-normoxia or EAE-CMH mice at the peak symptomatic phase of EAE were stained for CD31 (AlexaFluor-488) and VCAM-1 (Cy-3) in panel A or CD31 (Cy-3) and ICAM-1 (AlexaFluor-488) in panel C. Scale bar = 100 μm (inset, scale bar = 50 μm). b and d . Quantification of VCAM-1 ( b ) and ICAM-1 expression ( d ). Results are expressed as the mean ± SEM ( n = 6 mice/group). Note that CMH markedly suppressed vascular expression of VCAM-1 and ICAM-1. ** p
Figure Legend Snippet: CMH suppresses endothelial VCAM-1 and ICAM-1 expression during EAE. a and c . Frozen sections of lumbar spinal cord taken from disease-free, EAE-normoxia or EAE-CMH mice at the peak symptomatic phase of EAE were stained for CD31 (AlexaFluor-488) and VCAM-1 (Cy-3) in panel A or CD31 (Cy-3) and ICAM-1 (AlexaFluor-488) in panel C. Scale bar = 100 μm (inset, scale bar = 50 μm). b and d . Quantification of VCAM-1 ( b ) and ICAM-1 expression ( d ). Results are expressed as the mean ± SEM ( n = 6 mice/group). Note that CMH markedly suppressed vascular expression of VCAM-1 and ICAM-1. ** p

Techniques Used: Expressing, Mouse Assay, Staining

2) Product Images from "Comparative Study of Brain CD8+ T Cells Induced by Sporozoites and Those Induced by Blood-Stage Plasmodium berghei ANKA Involved in the Development of Cerebral Malaria "

Article Title: Comparative Study of Brain CD8+ T Cells Induced by Sporozoites and Those Induced by Blood-Stage Plasmodium berghei ANKA Involved in the Development of Cerebral Malaria

Journal: Infection and Immunity

doi: 10.1128/IAI.72.5.2817-2826.2004

Phenotype of CD8 + T lymphocytes isolated from the brains of CM + mice. (A) Activation markers. Lymphoid cells isolated from brains of CM + mice were doubly stained with anti-CD8 followed by anti-activation marker antibodies: CD25, CD44, CD62L, and CD69. Shown is a dot plot analysis indicating the activation markers expressed on naive cells from the LN of uninfected C57BL/6 mice (first row), CM + mice infected with PRBC (second row), and CM + mice infected with sporozoites (third row). (B) Adhesion molecules. The level of expression of the adhesion molecules on pooled lymphoid cells isolated from the brains of PRBC-infected CM + mice after double staining with CD8 and ICAM-1 or LFA-1 (solid lines) was compared with that on naive T CD8 + cells isolated from the blood (dotted lines).
Figure Legend Snippet: Phenotype of CD8 + T lymphocytes isolated from the brains of CM + mice. (A) Activation markers. Lymphoid cells isolated from brains of CM + mice were doubly stained with anti-CD8 followed by anti-activation marker antibodies: CD25, CD44, CD62L, and CD69. Shown is a dot plot analysis indicating the activation markers expressed on naive cells from the LN of uninfected C57BL/6 mice (first row), CM + mice infected with PRBC (second row), and CM + mice infected with sporozoites (third row). (B) Adhesion molecules. The level of expression of the adhesion molecules on pooled lymphoid cells isolated from the brains of PRBC-infected CM + mice after double staining with CD8 and ICAM-1 or LFA-1 (solid lines) was compared with that on naive T CD8 + cells isolated from the blood (dotted lines).

Techniques Used: Isolation, Mouse Assay, Activation Assay, Staining, Marker, Infection, Expressing, Double Staining

3) Product Images from "High-Multiplicity HIV-1 Infection and Neutralizing Antibody Evasion Mediated by the Macrophage-T Cell Virological Synapse"

Article Title: High-Multiplicity HIV-1 Infection and Neutralizing Antibody Evasion Mediated by the Macrophage-T Cell Virological Synapse

Journal: Journal of Virology

doi: 10.1128/JVI.03245-13

HIV-1 transmission requires Env receptor- and actin-dependent interactions. (A) Preincubation of CD4 + T cells with blocking anti-CD4 (13B8.2) or anti-CCR5 (2D7) antibody (10 μg/ml) or preincubation of HIV-1 BaL -infected MDM with anti-gp120 (2G12 or b12; 10 μg/ml) after Fc block resulted in a significant reduction in HIV-1 transfer to CD4 + T cells during 3 h of coculture. All MAbs were maintained during coculture. Transfer was measured by flow cytometry (FACSCalibur) of aspirated CD4 + T cells stained for CD3 and HIV-1 Gag, expressed as a percentage of the CD3 + Gag + cells in relevant isotype (mouse or human) control wells. (B) Preincubation of CD4 + T cells with blocking anti-LFA-1 (L130 n = 5 donors) or preincubation of HIV-1 BaL -infected MDM with anti-ICAM-1 (LB-2; n = 5 donors), ICAM-2 (B-T1; 10 μg/ml), or ICAM-3 (101-1D2; 10 μg/ml; both n = 2 donors) after Fc block followed by assessment of HIV-1 transfer to CD4 + T cells during 3 h of coculture with HIV-1 BaL -infected MDM. All MAbs were maintained during coculture. Transfer was measured as described for panel A and expressed as a percentage of the CD3 + Gag + cells in isotype control wells. Bars, means ± SEM. ***, P
Figure Legend Snippet: HIV-1 transmission requires Env receptor- and actin-dependent interactions. (A) Preincubation of CD4 + T cells with blocking anti-CD4 (13B8.2) or anti-CCR5 (2D7) antibody (10 μg/ml) or preincubation of HIV-1 BaL -infected MDM with anti-gp120 (2G12 or b12; 10 μg/ml) after Fc block resulted in a significant reduction in HIV-1 transfer to CD4 + T cells during 3 h of coculture. All MAbs were maintained during coculture. Transfer was measured by flow cytometry (FACSCalibur) of aspirated CD4 + T cells stained for CD3 and HIV-1 Gag, expressed as a percentage of the CD3 + Gag + cells in relevant isotype (mouse or human) control wells. (B) Preincubation of CD4 + T cells with blocking anti-LFA-1 (L130 n = 5 donors) or preincubation of HIV-1 BaL -infected MDM with anti-ICAM-1 (LB-2; n = 5 donors), ICAM-2 (B-T1; 10 μg/ml), or ICAM-3 (101-1D2; 10 μg/ml; both n = 2 donors) after Fc block followed by assessment of HIV-1 transfer to CD4 + T cells during 3 h of coculture with HIV-1 BaL -infected MDM. All MAbs were maintained during coculture. Transfer was measured as described for panel A and expressed as a percentage of the CD3 + Gag + cells in isotype control wells. Bars, means ± SEM. ***, P

Techniques Used: Transmission Assay, Blocking Assay, Infection, Flow Cytometry, Cytometry, Staining

4) Product Images from "HIV gp120 induces endothelial dysfunction in tumour necrosis factor-?-activated porcine and human endothelial cells"

Article Title: HIV gp120 induces endothelial dysfunction in tumour necrosis factor-?-activated porcine and human endothelial cells

Journal: Cardiovascular Research

doi: 10.1093/cvr/cvq013

Expression of ICAM-1 and HIV receptors/coreceptors and role of ICAM-1 silencing in HCAECs. ( A ) HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h, and the expression of ICAM-1 and HIV receptors or coreceptors including CD4, CXCR4, CCR5,
Figure Legend Snippet: Expression of ICAM-1 and HIV receptors/coreceptors and role of ICAM-1 silencing in HCAECs. ( A ) HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h, and the expression of ICAM-1 and HIV receptors or coreceptors including CD4, CXCR4, CCR5,

Techniques Used: Expressing

Effects of HIV gp120, TNF-α, anti-gp120, and anti-ICAM-1 antibodies on eNOS expression in HCAECs. Cells were pretreated with TNF-α for 8 h and followed by HIV gp120, HIV gp120 plus anti-gp120 antibody or HIV gp120 plus anti-ICAM-1 antibody
Figure Legend Snippet: Effects of HIV gp120, TNF-α, anti-gp120, and anti-ICAM-1 antibodies on eNOS expression in HCAECs. Cells were pretreated with TNF-α for 8 h and followed by HIV gp120, HIV gp120 plus anti-gp120 antibody or HIV gp120 plus anti-ICAM-1 antibody

Techniques Used: Expressing

Blocking effects of anti-gp120 and anti-ICAM-1 antibodies on HIV gp120-induced decrease in vasomotor function and eNOS expression in TNF-α-pretreated porcine coronary arteries. Porcine coronary artery rings were treated with TNF-α for
Figure Legend Snippet: Blocking effects of anti-gp120 and anti-ICAM-1 antibodies on HIV gp120-induced decrease in vasomotor function and eNOS expression in TNF-α-pretreated porcine coronary arteries. Porcine coronary artery rings were treated with TNF-α for

Techniques Used: Blocking Assay, Expressing

Effects of HIV gp120 and TNF-α on the immunoreactivity of eNOS and ICAM-1 in porcine coronary arteries. Porcine coronary artery rings were treated with TNF-α for 8 h and/or HIV gp120 for 16 h. Porcine coronary artery rings were fixed in
Figure Legend Snippet: Effects of HIV gp120 and TNF-α on the immunoreactivity of eNOS and ICAM-1 in porcine coronary arteries. Porcine coronary artery rings were treated with TNF-α for 8 h and/or HIV gp120 for 16 h. Porcine coronary artery rings were fixed in

Techniques Used:

5) Product Images from "The volatile anesthetic isoflurane perturbs conformational activation of integrin LFA-1 by binding to the allosteric regulatory cavity"

Article Title: The volatile anesthetic isoflurane perturbs conformational activation of integrin LFA-1 by binding to the allosteric regulatory cavity

Journal: The FASEB Journal

doi: 10.1096/fj.08-113324

NMR spectroscopy to study isoflurane-binding sites in the LFA-1 I domain. A ) Overlay experiments of 1 H, 15 N-HSQC acquired without (blue) and with (red) 12 mM isoflurane. Inset: isoflurane titration series of T291 (top right) and S245 (bottom left). Colors correspond to: 0 mM (blue), 3 mM (purple), 6 mM (orange), 9 mM (yellow), and 12 mM (red) isoflurane. B ) Scaled chemical-shift perturbation of 12 mM isoflurane mapped onto the LFA-1 I domain protein sequence and secondary structure. Chemical-shift perturbation calculated as [0.2(δ N iso − δ N 0 ) 2 +(δ H iso − δ H 0 ) 2 ] 1/2 . Inset residues from A . C ) showing amide nitrogen residues affected (δ ppm ≥0.05 ppm) by the addition of 12 mM isoflurane. Gray represents residues unperturbed by isoflurane; red represents residues that met or exceeded the threshold for perturbation. Helices and strands are labeled. Residues T291 (red) and S245 (green) are labeled. Yellow spheres represent the Mg 2+ ion at the ICAM-1 binding site, termed the metal ion-dependent adhesion site (MIDAS). Note that the residues near the MIADS were not affected and that the affected residues clustered near the cavity formed between the α1 and α7 helices and the central β strands. This figure was created using PYMOL.
Figure Legend Snippet: NMR spectroscopy to study isoflurane-binding sites in the LFA-1 I domain. A ) Overlay experiments of 1 H, 15 N-HSQC acquired without (blue) and with (red) 12 mM isoflurane. Inset: isoflurane titration series of T291 (top right) and S245 (bottom left). Colors correspond to: 0 mM (blue), 3 mM (purple), 6 mM (orange), 9 mM (yellow), and 12 mM (red) isoflurane. B ) Scaled chemical-shift perturbation of 12 mM isoflurane mapped onto the LFA-1 I domain protein sequence and secondary structure. Chemical-shift perturbation calculated as [0.2(δ N iso − δ N 0 ) 2 +(δ H iso − δ H 0 ) 2 ] 1/2 . Inset residues from A . C ) showing amide nitrogen residues affected (δ ppm ≥0.05 ppm) by the addition of 12 mM isoflurane. Gray represents residues unperturbed by isoflurane; red represents residues that met or exceeded the threshold for perturbation. Helices and strands are labeled. Residues T291 (red) and S245 (green) are labeled. Yellow spheres represent the Mg 2+ ion at the ICAM-1 binding site, termed the metal ion-dependent adhesion site (MIDAS). Note that the residues near the MIADS were not affected and that the affected residues clustered near the cavity formed between the α1 and α7 helices and the central β strands. This figure was created using PYMOL.

Techniques Used: Nuclear Magnetic Resonance, Spectroscopy, Binding Assay, Titration, Sequencing, Labeling

6) Product Images from "IL-11 Induces Encephalitogenic Th17 Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis"

Article Title: IL-11 Induces Encephalitogenic Th17 Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis

Journal: The Journal of Immunology Author Choice

doi: 10.4049/jimmunol.1900311

IL-11 induces Th17 cell response in RREAE. ( A ) SJL/J mice were immunized with PLP 139–151 peptide. On day 12 postimmunization, six mice per group were i.p. injected with recombinant mouse IL-11 (0.5 μg/mouse) or vehicle control. After 16 h, the mice were sacrificed and tissues were harvested. The cells were stimulated with PMA and ionomycin for intracellular staining, and the percentage of cells expressing each molecule was determined in gated CD4 + T cells. ( B ) Representative staining. ( C ) The percentage of CCR6-expressing cells in gated IL-17A + CD4 + cells. ( D ) The concentration of IL-17A in serum samples was measured by ELISA. ( E ) On day 56 postimmunization, six mice per group received recombinant mouse IL-11 (0.5 μg/mouse) or control vehicle. After 16 h, the mice were sacrificed. The percentage of IL-17A + cells was determined in gated CD4 + T cells from the PBMCs, spleen, and spinal cord inflammatory infiltrates. The percentage of ICAM-1 + cells was determined in gated CD4 + T cells from brain cell infiltrates. ( F ) The gene expression of IL-11 in LN and IL-17A in brain inflammatory infiltrates was detected by RT-PCR. ( G ) The concentration of IL-17A in the serum samples was measured by ELISA. ( H ) The percentages of ICAM-1 + cells were determined in gated IL-11 + CD4 + T cells from the brain and spinal cord cell infiltrates. The percentage of CCR6 + cells was determined in IL-11 + CD4 + T cells from the spinal cord infiltrates. The results are presented as mean ± SD per group. Statistical analysis was performed using a two-tailed paired Student t test. Each experiment was performed once.
Figure Legend Snippet: IL-11 induces Th17 cell response in RREAE. ( A ) SJL/J mice were immunized with PLP 139–151 peptide. On day 12 postimmunization, six mice per group were i.p. injected with recombinant mouse IL-11 (0.5 μg/mouse) or vehicle control. After 16 h, the mice were sacrificed and tissues were harvested. The cells were stimulated with PMA and ionomycin for intracellular staining, and the percentage of cells expressing each molecule was determined in gated CD4 + T cells. ( B ) Representative staining. ( C ) The percentage of CCR6-expressing cells in gated IL-17A + CD4 + cells. ( D ) The concentration of IL-17A in serum samples was measured by ELISA. ( E ) On day 56 postimmunization, six mice per group received recombinant mouse IL-11 (0.5 μg/mouse) or control vehicle. After 16 h, the mice were sacrificed. The percentage of IL-17A + cells was determined in gated CD4 + T cells from the PBMCs, spleen, and spinal cord inflammatory infiltrates. The percentage of ICAM-1 + cells was determined in gated CD4 + T cells from brain cell infiltrates. ( F ) The gene expression of IL-11 in LN and IL-17A in brain inflammatory infiltrates was detected by RT-PCR. ( G ) The concentration of IL-17A in the serum samples was measured by ELISA. ( H ) The percentages of ICAM-1 + cells were determined in gated IL-11 + CD4 + T cells from the brain and spinal cord cell infiltrates. The percentage of CCR6 + cells was determined in IL-11 + CD4 + T cells from the spinal cord infiltrates. The results are presented as mean ± SD per group. Statistical analysis was performed using a two-tailed paired Student t test. Each experiment was performed once.

Techniques Used: Mouse Assay, Plasmid Purification, Injection, Recombinant, Staining, Expressing, Concentration Assay, Enzyme-linked Immunosorbent Assay, Reverse Transcription Polymerase Chain Reaction, Two Tailed Test

7) Product Images from "Elevated levels of placental growth factor represent an adaptive host response in sepsis"

Article Title: Elevated levels of placental growth factor represent an adaptive host response in sepsis

Journal: The Journal of Experimental Medicine

doi: 10.1084/jem.20080398

Effect of PlGF deficiency on tissue mRNA/protein levels of inflammatory and hemostatic markers in a mouse model of endotoxemia. PLGF +/+ (WT) or PLGF −/− (KO) male mice were injected i.p. with or without 16 mg/kg LPS. (A) Shown are the results of quantitative real-time PCR analyses (mRNA copy number per 10 6 copies of 18S) of ICAM-1, VCAM-1, E-selectin, P-selectin, COX-2, and PAI-1 in the heart, lung and liver at 24 h. Data are expressed as means + SD of three independent experiments. *, P
Figure Legend Snippet: Effect of PlGF deficiency on tissue mRNA/protein levels of inflammatory and hemostatic markers in a mouse model of endotoxemia. PLGF +/+ (WT) or PLGF −/− (KO) male mice were injected i.p. with or without 16 mg/kg LPS. (A) Shown are the results of quantitative real-time PCR analyses (mRNA copy number per 10 6 copies of 18S) of ICAM-1, VCAM-1, E-selectin, P-selectin, COX-2, and PAI-1 in the heart, lung and liver at 24 h. Data are expressed as means + SD of three independent experiments. *, P

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

8) Product Images from "Antigen-specific transfer of CD40L to antigen-presenting B cells during T cell help"

Article Title: Antigen-specific transfer of CD40L to antigen-presenting B cells during T cell help

Journal: European journal of immunology

doi: 10.1002/eji.201646504

Antigen-specific CD40L transfer and help, unlike bystander help, is resistant to blocking by anti-CD40L antibody (A) Representative contour plot of CD40L transfer and ICAM-1 upregulation is shown for a single experiment in the antigen-pulsed B cells. Graph shows ICAM geometric mean fluorescent intensity values for CD40L positive and negative Ag-pulsed B cells after overnight incubation with Th1 cells in the presence of fluorescently labeled anti-CD40L antibody. p value was calculated using an unpaired, two-tailed Mann-Whitney test: p = 0.002 (B, C, D, E, F) Th1 and B cells were added to the top and bottom chambers of the Transwells® as depicted in the schematics in the presence (B) or absence (C, D, E, F) of fluorescently labeled anti-CD40L antibody. CD40L transfer (B) or ICAM-1 upregulation (C, D, E, F) was measured on the B cell populations in both the top and bottom chambers, and CD40L contour plots (B) or ICAM-1 histograms (C, D, E, F) are shown. The filled grey histogram on each panel is the control without antigen in the top chamber. This experiment is representative of two (B) or three (C, D, E, F) independent experiments. (G) Representative histograms of ICAM-1 upregulation on Ag+, Ag-, and no antigen control B cells after overnight incubation with 5CC7 Th1 cells. The graph shows the fold increase in ICAM-1 mean fluorescence intensity for three individual experiments (mean +/- SD) relative to the no Ag control B cell. (H, I left panel) Th1 cells were incubated with antigen-pulsed (Ag+) and bystander (Ag-) B cells in the presence or absence of neutralizing anti-CD40L antibody (10 μg/ml) and activation was assessed by ICAM upregulation. (I right panel) The graphs show the effects of different concentrations of anti-CD40L on activation of Ag+ and Ag- B cells. The left and right graphs are representative of three or two independent experiments, respectively. (J, K) Differentially labeled (CTV or CFSE) antigen-pulsed (Ag+) and CD40KO Ag+ along with Ag- B cells were incubated with Th1 cells, and proliferation was assessed after 48 hours by dilution of these dyes in the presence and absence of anti-CD40L (0.1 μg/ml). The percent of divided cells is labeled on each histogram and is representative of two independent experiments.
Figure Legend Snippet: Antigen-specific CD40L transfer and help, unlike bystander help, is resistant to blocking by anti-CD40L antibody (A) Representative contour plot of CD40L transfer and ICAM-1 upregulation is shown for a single experiment in the antigen-pulsed B cells. Graph shows ICAM geometric mean fluorescent intensity values for CD40L positive and negative Ag-pulsed B cells after overnight incubation with Th1 cells in the presence of fluorescently labeled anti-CD40L antibody. p value was calculated using an unpaired, two-tailed Mann-Whitney test: p = 0.002 (B, C, D, E, F) Th1 and B cells were added to the top and bottom chambers of the Transwells® as depicted in the schematics in the presence (B) or absence (C, D, E, F) of fluorescently labeled anti-CD40L antibody. CD40L transfer (B) or ICAM-1 upregulation (C, D, E, F) was measured on the B cell populations in both the top and bottom chambers, and CD40L contour plots (B) or ICAM-1 histograms (C, D, E, F) are shown. The filled grey histogram on each panel is the control without antigen in the top chamber. This experiment is representative of two (B) or three (C, D, E, F) independent experiments. (G) Representative histograms of ICAM-1 upregulation on Ag+, Ag-, and no antigen control B cells after overnight incubation with 5CC7 Th1 cells. The graph shows the fold increase in ICAM-1 mean fluorescence intensity for three individual experiments (mean +/- SD) relative to the no Ag control B cell. (H, I left panel) Th1 cells were incubated with antigen-pulsed (Ag+) and bystander (Ag-) B cells in the presence or absence of neutralizing anti-CD40L antibody (10 μg/ml) and activation was assessed by ICAM upregulation. (I right panel) The graphs show the effects of different concentrations of anti-CD40L on activation of Ag+ and Ag- B cells. The left and right graphs are representative of three or two independent experiments, respectively. (J, K) Differentially labeled (CTV or CFSE) antigen-pulsed (Ag+) and CD40KO Ag+ along with Ag- B cells were incubated with Th1 cells, and proliferation was assessed after 48 hours by dilution of these dyes in the presence and absence of anti-CD40L (0.1 μg/ml). The percent of divided cells is labeled on each histogram and is representative of two independent experiments.

Techniques Used: Blocking Assay, Incubation, Labeling, Two Tailed Test, MANN-WHITNEY, Fluorescence, Activation Assay

9) Product Images from "Tumor-Associated Endothelial Cells Promote Tumor Metastasis by Chaperoning Circulating Tumor Cells and Protecting Them from Anoikis"

Article Title: Tumor-Associated Endothelial Cells Promote Tumor Metastasis by Chaperoning Circulating Tumor Cells and Protecting Them from Anoikis

Journal: PLoS ONE

doi: 10.1371/journal.pone.0141602

Endothelial cells expressing Bcl-2 (EC-Bcl-2) show enhanced tumor cell binding. A-B; EC-Bcl-2 or EC-VC cells were cultured in 8-well chamber slides to form a uniform mono-layer. Tumor cells (CAL27 and UM-SCC-74B) were then pre-labeled with fluorescent dye (calcein-acetoxymethyl ester) and then added to endothelial cells and incubated for an additional 3 hours. At the end of incubation, cells were gently washed and photographed using Nikon Eclipse 80i microscope with DS-Ril camera. The scale bar represents 100 μm. C-D; tumor cell binding assays were performed in the presence or absence of neutralizing E-selectin, ICAM-1 or VCAM-1 antibodies. *, represent a significant increase and **, represent a significant decrease in adhesion molecule expression (p
Figure Legend Snippet: Endothelial cells expressing Bcl-2 (EC-Bcl-2) show enhanced tumor cell binding. A-B; EC-Bcl-2 or EC-VC cells were cultured in 8-well chamber slides to form a uniform mono-layer. Tumor cells (CAL27 and UM-SCC-74B) were then pre-labeled with fluorescent dye (calcein-acetoxymethyl ester) and then added to endothelial cells and incubated for an additional 3 hours. At the end of incubation, cells were gently washed and photographed using Nikon Eclipse 80i microscope with DS-Ril camera. The scale bar represents 100 μm. C-D; tumor cell binding assays were performed in the presence or absence of neutralizing E-selectin, ICAM-1 or VCAM-1 antibodies. *, represent a significant increase and **, represent a significant decrease in adhesion molecule expression (p

Techniques Used: Expressing, Binding Assay, Cell Culture, Labeling, Incubation, Microscopy

10) Product Images from "Targeted delivery of celastrol to mesangial cells is effective against mesangioproliferative glomerulonephritis"

Article Title: Targeted delivery of celastrol to mesangial cells is effective against mesangioproliferative glomerulonephritis

Journal: Nature Communications

doi: 10.1038/s41467-017-00834-8

Anti-inflammatory effects of CLT and CLT-AN in anti-Thy1.1 nephritic rats. a – d Real-time PCR analysis of renal mRNA levels of MCP-1 ( a ), ICAM-1 ( b ), IL-6 ( c ), IL-1β ( d ) in anti-Thy1.1 nephritic rats on day 1 after treatment with CLT or CLT-AN. Data are shown as normalized fold expressions relative to normal group using β-actin mRNA as internal control. e Representative photomicrographs of immunostaining for MCP-1, ICAM-1, IL-6, and IL-1β in kidney tissue sections taken from anti-Thy1.1 nephritic rats on day 1 after treatment with CLT or CLT-AN. Scale bars , 20 μm. f The levels of MCP-1, ICAM-1, IL-6, and IL-1β were semiquantitatively scored as described in Methods on the basis of immunohistochemical results. In panels a – d and f data are mean ± s.d. ( n = 5), results are representative of two independent experiments. * P
Figure Legend Snippet: Anti-inflammatory effects of CLT and CLT-AN in anti-Thy1.1 nephritic rats. a – d Real-time PCR analysis of renal mRNA levels of MCP-1 ( a ), ICAM-1 ( b ), IL-6 ( c ), IL-1β ( d ) in anti-Thy1.1 nephritic rats on day 1 after treatment with CLT or CLT-AN. Data are shown as normalized fold expressions relative to normal group using β-actin mRNA as internal control. e Representative photomicrographs of immunostaining for MCP-1, ICAM-1, IL-6, and IL-1β in kidney tissue sections taken from anti-Thy1.1 nephritic rats on day 1 after treatment with CLT or CLT-AN. Scale bars , 20 μm. f The levels of MCP-1, ICAM-1, IL-6, and IL-1β were semiquantitatively scored as described in Methods on the basis of immunohistochemical results. In panels a – d and f data are mean ± s.d. ( n = 5), results are representative of two independent experiments. * P

Techniques Used: Real-time Polymerase Chain Reaction, Immunostaining, Immunohistochemistry

11) Product Images from "Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection"

Article Title: Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection

Journal: Respiratory Research

doi: 10.1186/1465-9921-7-71

Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.
Figure Legend Snippet: Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.

Techniques Used: Expressing, Derivative Assay

12) Product Images from "Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection"

Article Title: Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection

Journal: Respiratory Research

doi: 10.1186/1465-9921-7-71

Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.
Figure Legend Snippet: Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.

Techniques Used: Expressing, Derivative Assay

13) Product Images from "Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection"

Article Title: Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection

Journal: Respiratory Research

doi: 10.1186/1465-9921-7-71

Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.
Figure Legend Snippet: Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.

Techniques Used: Expressing, Derivative Assay

14) Product Images from "Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection"

Article Title: Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection

Journal: Respiratory Research

doi: 10.1186/1465-9921-7-71

Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.
Figure Legend Snippet: Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.

Techniques Used: Expressing, Derivative Assay

15) Product Images from "Atomic Force Microscopy Reveals a Role for Endothelial Cell ICAM-1 Expression in Bladder Cancer Cell Adherence"

Article Title: Atomic Force Microscopy Reveals a Role for Endothelial Cell ICAM-1 Expression in Bladder Cancer Cell Adherence

Journal: PLoS ONE

doi: 10.1371/journal.pone.0098034

ICAM-1 is involved in the interaction between cancer cells and ECs. Rupture force vs. retraction speed after interaction between cancer cell and an EC, treated with an anti ICAM-1 antibody or not. Corresponding box-whisker plots show rupture forces at a retraction speed of 5 µm/s. (A, B) T24-EC, (C, D) J82-EC and (E, F) RT112-EC. As a comparison, the rupture force box plot is also shown for the T24-BSA interaction (panel G). For panels A, C and E, the line is just a guide for the eye. Data are plotted as mean ± standard error of the mean. Stars represent the p-value from GLMM statistical tests between parameters calculated on untreated and anti-ICAM-1-treated cells (*p≤0.05).
Figure Legend Snippet: ICAM-1 is involved in the interaction between cancer cells and ECs. Rupture force vs. retraction speed after interaction between cancer cell and an EC, treated with an anti ICAM-1 antibody or not. Corresponding box-whisker plots show rupture forces at a retraction speed of 5 µm/s. (A, B) T24-EC, (C, D) J82-EC and (E, F) RT112-EC. As a comparison, the rupture force box plot is also shown for the T24-BSA interaction (panel G). For panels A, C and E, the line is just a guide for the eye. Data are plotted as mean ± standard error of the mean. Stars represent the p-value from GLMM statistical tests between parameters calculated on untreated and anti-ICAM-1-treated cells (*p≤0.05).

Techniques Used: Whisker Assay

Control experiments for T24 cells interacting with recombinant ICAM-1 or BSA coated surfaces. Rupture force vs. retraction speed for T24 cells interacting either with a coated substrate or with ECs (circle). The substrate is coated with BSA 100 µg/ml (square) or recombinant ICAM-1 25 µg/ml (diamond). Data are plotted as mean ± standard error of the mean. The line is just a guide for the eye.
Figure Legend Snippet: Control experiments for T24 cells interacting with recombinant ICAM-1 or BSA coated surfaces. Rupture force vs. retraction speed for T24 cells interacting either with a coated substrate or with ECs (circle). The substrate is coated with BSA 100 µg/ml (square) or recombinant ICAM-1 25 µg/ml (diamond). Data are plotted as mean ± standard error of the mean. The line is just a guide for the eye.

Techniques Used: Recombinant

Distribution of rupture forces and effect of an anti-ICAM-1 antibody. Effect of an anti-ICAM-1 antibody on cancer-EC interactions. Rupture force distributions are Gaussian with one or two peaks revealing the presence of receptor/ligand bonds or non specific interactions. Probability histograms of rupture force (V = 5 µm/s) for (A) T24-HUVEC, (B) J82-HUVEC, (C) RT112-HUVEC. Black histograms represent interaction cancer-cell and EC without antibody whereas red ones show the force distribution after using the antibody. Panels D (T24-ICAM-1) and E (T24-BSA) show the rupture force probabilities for T24 cells in contact with coated substrates. The number N of events is indicated on the histograms.
Figure Legend Snippet: Distribution of rupture forces and effect of an anti-ICAM-1 antibody. Effect of an anti-ICAM-1 antibody on cancer-EC interactions. Rupture force distributions are Gaussian with one or two peaks revealing the presence of receptor/ligand bonds or non specific interactions. Probability histograms of rupture force (V = 5 µm/s) for (A) T24-HUVEC, (B) J82-HUVEC, (C) RT112-HUVEC. Black histograms represent interaction cancer-cell and EC without antibody whereas red ones show the force distribution after using the antibody. Panels D (T24-ICAM-1) and E (T24-BSA) show the rupture force probabilities for T24 cells in contact with coated substrates. The number N of events is indicated on the histograms.

Techniques Used:

ICAM-1 expression on ECs. A ) Confocal microscopy image of an EC monolayer stained for ICAM-1 (green). HUVECs were fixed with PFA. Nuclei are stained in blue using DAPI. B ) Quantification of ICAM-1 levels by FACS analysis (dashed line) in comparison with an irrelevant antibody (solid line).
Figure Legend Snippet: ICAM-1 expression on ECs. A ) Confocal microscopy image of an EC monolayer stained for ICAM-1 (green). HUVECs were fixed with PFA. Nuclei are stained in blue using DAPI. B ) Quantification of ICAM-1 levels by FACS analysis (dashed line) in comparison with an irrelevant antibody (solid line).

Techniques Used: Expressing, Confocal Microscopy, Staining, FACS

16) Product Images from "Knockdown of TNFR1 by the sense strand of an ICAM-1 siRNA: dissection of an off-target effect"

Article Title: Knockdown of TNFR1 by the sense strand of an ICAM-1 siRNA: dissection of an off-target effect

Journal: Nucleic Acids Research

doi: 10.1093/nar/gkm630

2′- O -methyl modification of the 736 sense strand eliminates TNFR1 knockdown. ( A ) Hybrid 736 siRNA duplexes were prepared by annealing unmodified 736 RNA oligos (sense or antisense) with complementary RNA oligos modified by 2′- O -methylation, (such hybrid duplexes are indicated as 736/S or 736/AS). Dual modified duplexes (736/S+AS) and wild-type 736 (736/WT) were also prepared. 2′- O -Me modified bases are in bold and underlined. ( B ) HUVEC were mock-transfected or transfected with 10 nM LFA-3, an irrelevant siRNA, 736/WT, 736/S, 736/AS or 736/S + AS siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for ICAM-1 and E-selectin and analyzed by flow cytometry. Corrected MFIs were converted to ‘% Remaining’ relative to mock expression. ( C ) Hybrid siRNA-transfected HUVEC lysates were analyzed by western blot for the expression of TNFR1 and β-actin. Representative of one of two experiments with similar results.
Figure Legend Snippet: 2′- O -methyl modification of the 736 sense strand eliminates TNFR1 knockdown. ( A ) Hybrid 736 siRNA duplexes were prepared by annealing unmodified 736 RNA oligos (sense or antisense) with complementary RNA oligos modified by 2′- O -methylation, (such hybrid duplexes are indicated as 736/S or 736/AS). Dual modified duplexes (736/S+AS) and wild-type 736 (736/WT) were also prepared. 2′- O -Me modified bases are in bold and underlined. ( B ) HUVEC were mock-transfected or transfected with 10 nM LFA-3, an irrelevant siRNA, 736/WT, 736/S, 736/AS or 736/S + AS siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for ICAM-1 and E-selectin and analyzed by flow cytometry. Corrected MFIs were converted to ‘% Remaining’ relative to mock expression. ( C ) Hybrid siRNA-transfected HUVEC lysates were analyzed by western blot for the expression of TNFR1 and β-actin. Representative of one of two experiments with similar results.

Techniques Used: Modification, Methylation, Transfection, Staining, Flow Cytometry, Cytometry, Expressing, Western Blot

736 Inhibits TNF-mediated HUVEC antigen expression. HUVEC were mock-transfected or transfected with 10 nM 736 or lamin siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for E-selectin, ICAM-1, VCAM-1 and MHC I and analyzed by flow cytometry. Filled histograms represent antigen-specific staining and empty histograms represent isotype control staining. Corrected MFI in the upper right hand corner = antigen-specific MFI minus isotype MFI. Representative of one of three experiments with similar results.
Figure Legend Snippet: 736 Inhibits TNF-mediated HUVEC antigen expression. HUVEC were mock-transfected or transfected with 10 nM 736 or lamin siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for E-selectin, ICAM-1, VCAM-1 and MHC I and analyzed by flow cytometry. Filled histograms represent antigen-specific staining and empty histograms represent isotype control staining. Corrected MFI in the upper right hand corner = antigen-specific MFI minus isotype MFI. Representative of one of three experiments with similar results.

Techniques Used: Expressing, Transfection, Staining, Flow Cytometry, Cytometry

736 siRNA selectively targets TNFR1 mRNA and protein and selectively inhibits TNF responses. ( A ) HUVEC were mock-transfected or transfected with 736 or lamin siRNA. Cell lysates were prepared 24 h after the last transfection, resolved by SDS-PAGE, and immunoblotted with antibodies specific for TNF receptor signaling proteins. ( B ) HUVEC were transfected with 736 or lamin siRNA. cDNA from each culture was analyzed by qRT-PCR using TNF signalosome-specific primers. Values were normalized using actin controls and converted to ‘% mRNA Remaining’ relative to mock expression levels. Representative of one of two experiments with similar results. ( C ) HUVEC were transfected with 736 or lamin siRNA. Cells were then stimulated for 24 h with either TNF (10 ng/ml) or IL-1β (50 ng/ml), immuno-stained using fluorescent antigen-specific antibody for ICAM-1 and analyzed by flow cytometry.
Figure Legend Snippet: 736 siRNA selectively targets TNFR1 mRNA and protein and selectively inhibits TNF responses. ( A ) HUVEC were mock-transfected or transfected with 736 or lamin siRNA. Cell lysates were prepared 24 h after the last transfection, resolved by SDS-PAGE, and immunoblotted with antibodies specific for TNF receptor signaling proteins. ( B ) HUVEC were transfected with 736 or lamin siRNA. cDNA from each culture was analyzed by qRT-PCR using TNF signalosome-specific primers. Values were normalized using actin controls and converted to ‘% mRNA Remaining’ relative to mock expression levels. Representative of one of two experiments with similar results. ( C ) HUVEC were transfected with 736 or lamin siRNA. Cells were then stimulated for 24 h with either TNF (10 ng/ml) or IL-1β (50 ng/ml), immuno-stained using fluorescent antigen-specific antibody for ICAM-1 and analyzed by flow cytometry.

Techniques Used: Transfection, SDS Page, Quantitative RT-PCR, Expressing, Staining, Flow Cytometry, Cytometry

5′ phosphorylation of the 736 sense strand is required for effective TNFR1 knockdown. Hybrid 736 siRNA duplexes were prepared by annealing wild-type 736 antisense RNA oligos with either wild-type 736 sense strand oligos [736 (WT)] or 5′deoxy capped 736 sense strand oligos [736 (5′Cap)]. HUVEC were mock-transfected or transfected with 10 nM lamin, 736 (WT), or 736 (5′Cap) siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for E-selectin and ICAM-1 and analyzed by flow cytometry. Filled histograms represent antigen-specific staining and empty histograms represent isotype control staining. Corrected MFI in the upper right hand corner = antigen-specific MFI minus isotype MFI. Representative of one of two experiments with similar results.
Figure Legend Snippet: 5′ phosphorylation of the 736 sense strand is required for effective TNFR1 knockdown. Hybrid 736 siRNA duplexes were prepared by annealing wild-type 736 antisense RNA oligos with either wild-type 736 sense strand oligos [736 (WT)] or 5′deoxy capped 736 sense strand oligos [736 (5′Cap)]. HUVEC were mock-transfected or transfected with 10 nM lamin, 736 (WT), or 736 (5′Cap) siRNA on consecutive days and treated with 10 ng/ml TNF for 24 h. HUVEC were immuno-stained using fluorescent antigen-specific antibodies for E-selectin and ICAM-1 and analyzed by flow cytometry. Filled histograms represent antigen-specific staining and empty histograms represent isotype control staining. Corrected MFI in the upper right hand corner = antigen-specific MFI minus isotype MFI. Representative of one of two experiments with similar results.

Techniques Used: Transfection, Staining, Flow Cytometry, Cytometry

Complementarity between TNFR1 and ICAM-1 does not activate a natural antisense transcript (NAT) activity. ( A ) HUVEC cell lines expressing EGFP/TNFR1 3′UTR chimeric constructs were treated for 24 h with increasing concentrations of TNF to induce ICAM-1 expression. ICAM-1 expression levels were determined by FACS using an ICAM-1-specific antibody. ( B ) HDMEC cell lines overexpressing E-selectin and ICAM-1 were tested to determine basal TNFR1 cell surface levels. Cells were immunostained with fluorescently labeled antibody specific for ICAM-1, TNFR1 and TNFR2 then analyzed by FACS. Representative of one of two independent experiments with similar results.
Figure Legend Snippet: Complementarity between TNFR1 and ICAM-1 does not activate a natural antisense transcript (NAT) activity. ( A ) HUVEC cell lines expressing EGFP/TNFR1 3′UTR chimeric constructs were treated for 24 h with increasing concentrations of TNF to induce ICAM-1 expression. ICAM-1 expression levels were determined by FACS using an ICAM-1-specific antibody. ( B ) HDMEC cell lines overexpressing E-selectin and ICAM-1 were tested to determine basal TNFR1 cell surface levels. Cells were immunostained with fluorescently labeled antibody specific for ICAM-1, TNFR1 and TNFR2 then analyzed by FACS. Representative of one of two independent experiments with similar results.

Techniques Used: Activity Assay, Expressing, Construct, FACS, Labeling

17) Product Images from "Isolation and characterization of human primary enterocytes from small intestine using a novel method"

Article Title: Isolation and characterization of human primary enterocytes from small intestine using a novel method

Journal: Scandinavian Journal of Gastroenterology

doi: 10.3109/00365521.2012.708940

Flow cytometric analysis of cultured human EpCAM-positive cells. (A) Flow cytometric results are presented in the form of histograms. Representative histograms for expression of TLRs in enterocytes are shown. Primary enterocytes did not express TLR-1, -2, -3, -4 and -9. They weakly expressed TLR-5, but demonstrated strong expression of TLR-6, -7, -8 and -10. The expression of TLRs was observed only in saponin-treated cells. (B) Isolated human enterocytes also stained positive for several immune recognition molecules such as CD44, CD86, ICAM-1 and CD40. Staining with only the secondary antibody served as negative control (grey filled histogram).
Figure Legend Snippet: Flow cytometric analysis of cultured human EpCAM-positive cells. (A) Flow cytometric results are presented in the form of histograms. Representative histograms for expression of TLRs in enterocytes are shown. Primary enterocytes did not express TLR-1, -2, -3, -4 and -9. They weakly expressed TLR-5, but demonstrated strong expression of TLR-6, -7, -8 and -10. The expression of TLRs was observed only in saponin-treated cells. (B) Isolated human enterocytes also stained positive for several immune recognition molecules such as CD44, CD86, ICAM-1 and CD40. Staining with only the secondary antibody served as negative control (grey filled histogram).

Techniques Used: Flow Cytometry, Cell Culture, Expressing, Isolation, Staining, Negative Control

18) Product Images from "Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection"

Article Title: Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection

Journal: Respiratory Research

doi: 10.1186/1465-9921-7-71

Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.
Figure Legend Snippet: Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.

Techniques Used: Expressing, Derivative Assay

19) Product Images from "Atomic Force Microscopy Reveals a Role for Endothelial Cell ICAM-1 Expression in Bladder Cancer Cell Adherence"

Article Title: Atomic Force Microscopy Reveals a Role for Endothelial Cell ICAM-1 Expression in Bladder Cancer Cell Adherence

Journal: PLoS ONE

doi: 10.1371/journal.pone.0098034

ICAM-1 is involved in the interaction between cancer cells and ECs. Rupture force vs. retraction speed after interaction between cancer cell and an EC, treated with an anti ICAM-1 antibody or not. Corresponding box-whisker plots show rupture forces at a retraction speed of 5 µm/s. (A, B) T24-EC, (C, D) J82-EC and (E, F) RT112-EC. As a comparison, the rupture force box plot is also shown for the T24-BSA interaction (panel G). For panels A, C and E, the line is just a guide for the eye. Data are plotted as mean ± standard error of the mean. Stars represent the p-value from GLMM statistical tests between parameters calculated on untreated and anti-ICAM-1-treated cells (*p≤0.05).
Figure Legend Snippet: ICAM-1 is involved in the interaction between cancer cells and ECs. Rupture force vs. retraction speed after interaction between cancer cell and an EC, treated with an anti ICAM-1 antibody or not. Corresponding box-whisker plots show rupture forces at a retraction speed of 5 µm/s. (A, B) T24-EC, (C, D) J82-EC and (E, F) RT112-EC. As a comparison, the rupture force box plot is also shown for the T24-BSA interaction (panel G). For panels A, C and E, the line is just a guide for the eye. Data are plotted as mean ± standard error of the mean. Stars represent the p-value from GLMM statistical tests between parameters calculated on untreated and anti-ICAM-1-treated cells (*p≤0.05).

Techniques Used: Whisker Assay

Control experiments for T24 cells interacting with recombinant ICAM-1 or BSA coated surfaces. Rupture force vs. retraction speed for T24 cells interacting either with a coated substrate or with ECs (circle). The substrate is coated with BSA 100 µg/ml (square) or recombinant ICAM-1 25 µg/ml (diamond). Data are plotted as mean ± standard error of the mean. The line is just a guide for the eye.
Figure Legend Snippet: Control experiments for T24 cells interacting with recombinant ICAM-1 or BSA coated surfaces. Rupture force vs. retraction speed for T24 cells interacting either with a coated substrate or with ECs (circle). The substrate is coated with BSA 100 µg/ml (square) or recombinant ICAM-1 25 µg/ml (diamond). Data are plotted as mean ± standard error of the mean. The line is just a guide for the eye.

Techniques Used: Recombinant

Distribution of rupture forces and effect of an anti-ICAM-1 antibody. Effect of an anti-ICAM-1 antibody on cancer-EC interactions. Rupture force distributions are Gaussian with one or two peaks revealing the presence of receptor/ligand bonds or non specific interactions. Probability histograms of rupture force (V = 5 µm/s) for (A) T24-HUVEC, (B) J82-HUVEC, (C) RT112-HUVEC. Black histograms represent interaction cancer-cell and EC without antibody whereas red ones show the force distribution after using the antibody. Panels D (T24-ICAM-1) and E (T24-BSA) show the rupture force probabilities for T24 cells in contact with coated substrates. The number N of events is indicated on the histograms.
Figure Legend Snippet: Distribution of rupture forces and effect of an anti-ICAM-1 antibody. Effect of an anti-ICAM-1 antibody on cancer-EC interactions. Rupture force distributions are Gaussian with one or two peaks revealing the presence of receptor/ligand bonds or non specific interactions. Probability histograms of rupture force (V = 5 µm/s) for (A) T24-HUVEC, (B) J82-HUVEC, (C) RT112-HUVEC. Black histograms represent interaction cancer-cell and EC without antibody whereas red ones show the force distribution after using the antibody. Panels D (T24-ICAM-1) and E (T24-BSA) show the rupture force probabilities for T24 cells in contact with coated substrates. The number N of events is indicated on the histograms.

Techniques Used:

ICAM-1 expression on ECs. A ) Confocal microscopy image of an EC monolayer stained for ICAM-1 (green). HUVECs were fixed with PFA. Nuclei are stained in blue using DAPI. B ) Quantification of ICAM-1 levels by FACS analysis (dashed line) in comparison with an irrelevant antibody (solid line).
Figure Legend Snippet: ICAM-1 expression on ECs. A ) Confocal microscopy image of an EC monolayer stained for ICAM-1 (green). HUVECs were fixed with PFA. Nuclei are stained in blue using DAPI. B ) Quantification of ICAM-1 levels by FACS analysis (dashed line) in comparison with an irrelevant antibody (solid line).

Techniques Used: Expressing, Confocal Microscopy, Staining, FACS

20) Product Images from "Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection"

Article Title: Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection

Journal: Respiratory Research

doi: 10.1186/1465-9921-7-71

Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.
Figure Legend Snippet: Similar expression of ICAM-1 on asthmatic and non-asthmatic HASM cells . A typical histogram of the expression of cell surface ICAM-1 on HASM cells derived from asthmatic (black line) and non-asthmatic (blue line) donors. Isotype controls are represented by the red (solid filled) and green lines for the HASM cells derived from non-asthmatic and asthmatic donors respectively.

Techniques Used: Expressing, Derivative Assay

21) Product Images from "Zinc Finger Transcription Factors Designed for Bispecific Coregulation of ErbB2 and ErbB3 Receptors: Insights into ErbB Receptor Biology"

Article Title: Zinc Finger Transcription Factors Designed for Bispecific Coregulation of ErbB2 and ErbB3 Receptors: Insights into ErbB Receptor Biology

Journal: Molecular and Cellular Biology

doi: 10.1128/MCB.25.20.9082-9091.2005

FACS analysis of 12-finger ATF-expressing cells. (A) Flow cytometry analysis of A431 cells transduced with ATF KRAB-E3-15L-31OPT or E3-15L-31OPT-VP64. (B) Flow cytometry analyses of MDA-MB-436, SKOV-3, and A431 cells transduced with ATF KRAB-E2C-15L-E3. Three days after transduction, cells were stained with ErbB3-, ICAM-1- or ErbB2-specific primary antibodies, followed by a Cy5-labeled secondary antibody. In all panels, the thin line represents the background fluorescence distribution of A431 cells stained with the IgG1 isotype control antibody, the dotted line is the fluorescence distribution for the level of ErbB2, ErbB3, or ICAM-1 expressed by untransduced A431 cells, and the bold line is the fluorescence distribution of A431 cells transduced with the ATF indicated.
Figure Legend Snippet: FACS analysis of 12-finger ATF-expressing cells. (A) Flow cytometry analysis of A431 cells transduced with ATF KRAB-E3-15L-31OPT or E3-15L-31OPT-VP64. (B) Flow cytometry analyses of MDA-MB-436, SKOV-3, and A431 cells transduced with ATF KRAB-E2C-15L-E3. Three days after transduction, cells were stained with ErbB3-, ICAM-1- or ErbB2-specific primary antibodies, followed by a Cy5-labeled secondary antibody. In all panels, the thin line represents the background fluorescence distribution of A431 cells stained with the IgG1 isotype control antibody, the dotted line is the fluorescence distribution for the level of ErbB2, ErbB3, or ICAM-1 expressed by untransduced A431 cells, and the bold line is the fluorescence distribution of A431 cells transduced with the ATF indicated.

Techniques Used: FACS, Expressing, Flow Cytometry, Cytometry, Transduction, Multiple Displacement Amplification, Staining, Labeling, Fluorescence

22) Product Images from "Targeted delivery of celastrol to mesangial cells is effective against mesangioproliferative glomerulonephritis"

Article Title: Targeted delivery of celastrol to mesangial cells is effective against mesangioproliferative glomerulonephritis

Journal: Nature Communications

doi: 10.1038/s41467-017-00834-8

Anti-inflammatory effects of CLT and CLT-AN in anti-Thy1.1 nephritic rats. a – d Real-time PCR analysis of renal mRNA levels of MCP-1 ( a ), ICAM-1 ( b ), IL-6 ( c ), IL-1β ( d ) in anti-Thy1.1 nephritic rats on day 1 after treatment with CLT or CLT-AN. Data are shown as normalized fold expressions relative to normal group using β-actin mRNA as internal control. e Representative photomicrographs of immunostaining for MCP-1, ICAM-1, IL-6, and IL-1β in kidney tissue sections taken from anti-Thy1.1 nephritic rats on day 1 after treatment with CLT or CLT-AN. Scale bars , 20 μm. f The levels of MCP-1, ICAM-1, IL-6, and IL-1β were semiquantitatively scored as described in Methods on the basis of immunohistochemical results. In panels a – d and f data are mean ± s.d. ( n = 5), results are representative of two independent experiments. * P
Figure Legend Snippet: Anti-inflammatory effects of CLT and CLT-AN in anti-Thy1.1 nephritic rats. a – d Real-time PCR analysis of renal mRNA levels of MCP-1 ( a ), ICAM-1 ( b ), IL-6 ( c ), IL-1β ( d ) in anti-Thy1.1 nephritic rats on day 1 after treatment with CLT or CLT-AN. Data are shown as normalized fold expressions relative to normal group using β-actin mRNA as internal control. e Representative photomicrographs of immunostaining for MCP-1, ICAM-1, IL-6, and IL-1β in kidney tissue sections taken from anti-Thy1.1 nephritic rats on day 1 after treatment with CLT or CLT-AN. Scale bars , 20 μm. f The levels of MCP-1, ICAM-1, IL-6, and IL-1β were semiquantitatively scored as described in Methods on the basis of immunohistochemical results. In panels a – d and f data are mean ± s.d. ( n = 5), results are representative of two independent experiments. * P

Techniques Used: Real-time Polymerase Chain Reaction, Immunostaining, Immunohistochemistry

23) Product Images from "Dysregulation of Neutrophil CXCR2 and Pulmonary Endothelial ICAM-1 Promotes Age-Related Pulmonary Inflammation"

Article Title: Dysregulation of Neutrophil CXCR2 and Pulmonary Endothelial ICAM-1 Promotes Age-Related Pulmonary Inflammation

Journal: Aging and Disease

doi:

Pulmonary endothelial ICAM-1 expression after burn . Lung sections immunostained with anti-ICAM-1 (red) and anti-PECAM-1 (green) antibodies. ( A ) Representative images are shown from young and aged mice at 24 hours after sham or burn injury at 200x magnification.
Figure Legend Snippet: Pulmonary endothelial ICAM-1 expression after burn . Lung sections immunostained with anti-ICAM-1 (red) and anti-PECAM-1 (green) antibodies. ( A ) Representative images are shown from young and aged mice at 24 hours after sham or burn injury at 200x magnification.

Techniques Used: Expressing, Mouse Assay

24) Product Images from "Endothelial Adora2a Activation Promotes Blood–Brain Barrier Breakdown and Cognitive Impairment in Mice with Diet-Induced Insulin Resistance"

Article Title: Endothelial Adora2a Activation Promotes Blood–Brain Barrier Breakdown and Cognitive Impairment in Mice with Diet-Induced Insulin Resistance

Journal: The Journal of Neuroscience

doi: 10.1523/JNEUROSCI.2506-18.2019

Endothelial Adora2a is required for cerebrovascular inflammation in diabetic mice. A , Forebrain MVs were isolated from Tie2 rtTA /tetO cre /Adora2a fl/fl Tg mice and nTg littermates after 16 weeks of LFD or HFD. Cells were gated on forward and side scatter [shown in region 1 (R1)] and the activation markers e-selectin (CD62E) and ICAM-1 were measured in CD45−/CD31+ endothelial cells. For histograms, marker 1 (M1) denotes gating of CD45-negative cells and marker 2 (M2) indicates gating of CD31+ cells. B , Endothelial Adora2a ablation prevents induction of ICAM-1 in mice on HFD. C , Tg mice were protected against endothelial induction of CD62E on HFD. D , Representative scatter plots of CD62E in CD45-/CD31+ forebrain endothelial cells. Activated endothelial cells (CD31+/CD62E+) are shown in red and quiescent endothelial cells (CD31+/CD62E−) are shown in blue. Percentages (red text) reflect proportion of activated endothelial cells relative to total endothelial cells. E , qPCR analysis of adenosine receptor subtypes (Adora1, Adora2a), genes encoding tight junction proteins (Cldn1, Jam2), VEGF signaling genes (VEGF-A, VEGF-B, VEGFR1, VEGFR2), and glucose transporter 1 (Glut1) in MV preparations from nTg and Tg mice on HFD or LFD. F , Immunofluorescence visualization of the endothelial activation marker COX-2 in hippocampal sections. Scale bars: far left, 50 μm; (in nTg/LFD) for all other micrographs, 10 μm. B , C , Bar height represents the average of ( n = 6–8) mice per condition; E , bar height shows the average of ( n = 4–6) mice per condition. For all graphs, error bars represent SEM and asterisk (*) indicates significance at p
Figure Legend Snippet: Endothelial Adora2a is required for cerebrovascular inflammation in diabetic mice. A , Forebrain MVs were isolated from Tie2 rtTA /tetO cre /Adora2a fl/fl Tg mice and nTg littermates after 16 weeks of LFD or HFD. Cells were gated on forward and side scatter [shown in region 1 (R1)] and the activation markers e-selectin (CD62E) and ICAM-1 were measured in CD45−/CD31+ endothelial cells. For histograms, marker 1 (M1) denotes gating of CD45-negative cells and marker 2 (M2) indicates gating of CD31+ cells. B , Endothelial Adora2a ablation prevents induction of ICAM-1 in mice on HFD. C , Tg mice were protected against endothelial induction of CD62E on HFD. D , Representative scatter plots of CD62E in CD45-/CD31+ forebrain endothelial cells. Activated endothelial cells (CD31+/CD62E+) are shown in red and quiescent endothelial cells (CD31+/CD62E−) are shown in blue. Percentages (red text) reflect proportion of activated endothelial cells relative to total endothelial cells. E , qPCR analysis of adenosine receptor subtypes (Adora1, Adora2a), genes encoding tight junction proteins (Cldn1, Jam2), VEGF signaling genes (VEGF-A, VEGF-B, VEGFR1, VEGFR2), and glucose transporter 1 (Glut1) in MV preparations from nTg and Tg mice on HFD or LFD. F , Immunofluorescence visualization of the endothelial activation marker COX-2 in hippocampal sections. Scale bars: far left, 50 μm; (in nTg/LFD) for all other micrographs, 10 μm. B , C , Bar height represents the average of ( n = 6–8) mice per condition; E , bar height shows the average of ( n = 4–6) mice per condition. For all graphs, error bars represent SEM and asterisk (*) indicates significance at p

Techniques Used: Mouse Assay, Isolation, Activation Assay, Marker, Real-time Polymerase Chain Reaction, Immunofluorescence

25) Product Images from "Disialyl GD2 ganglioside suppresses ICAM-1-mediated invasiveness in human breast cancer MDA-MB231 cells"

Article Title: Disialyl GD2 ganglioside suppresses ICAM-1-mediated invasiveness in human breast cancer MDA-MB231 cells

Journal: International Journal of Biological Sciences

doi: 10.7150/ijbs.16903

Downregulation of ICAM-1 expression (A, B, C, D, E) in pc3-GD3s cells. Expression levels of ICAM-1 mRNA were checked by RT-PCR (A) and real-time PCR (B). Expression of ICAM-1 confirmed by Western blot (C) and FACS analysis (D). A schematic representation of DNA constructions containing two different forms of the ICAM-1 promters linked to the luciferase reporter gene is shown. The values represent the mean ±S.D. for three independent experiments with triplicate measurements (E). Inhibition of AKT phosphorylation in pc3-GD3s cells (F). Total protein extracts from pc3 and pc3-GD3s cells were examined by Western blot analysis with anti-phospho-AKT, anti-AKT, anti-phospho-ERK1/2, anti-ERK1/2, anti-phospho-p38 and anti-p38 antibodies. The nonspecific IgG antiserum has been used to block the cell reaction. GAPDH was included as an internal control. All experiments performed at least three times and we examined mean differences between groups by using the error bar graph procedure.
Figure Legend Snippet: Downregulation of ICAM-1 expression (A, B, C, D, E) in pc3-GD3s cells. Expression levels of ICAM-1 mRNA were checked by RT-PCR (A) and real-time PCR (B). Expression of ICAM-1 confirmed by Western blot (C) and FACS analysis (D). A schematic representation of DNA constructions containing two different forms of the ICAM-1 promters linked to the luciferase reporter gene is shown. The values represent the mean ±S.D. for three independent experiments with triplicate measurements (E). Inhibition of AKT phosphorylation in pc3-GD3s cells (F). Total protein extracts from pc3 and pc3-GD3s cells were examined by Western blot analysis with anti-phospho-AKT, anti-AKT, anti-phospho-ERK1/2, anti-ERK1/2, anti-phospho-p38 and anti-p38 antibodies. The nonspecific IgG antiserum has been used to block the cell reaction. GAPDH was included as an internal control. All experiments performed at least three times and we examined mean differences between groups by using the error bar graph procedure.

Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Real-time Polymerase Chain Reaction, Western Blot, FACS, Luciferase, Inhibition, Blocking Assay

Differential regulation of ICAM-1 expression in pc3-GD3s-trasnfected SK-BR3 (ER-) and MCF-7 (ER+) cells. Expression levels of GM3 synthase, GD3 synthase and ICAM-1 mRNAs in the pc3-GD3s-transfected SK-BR3 (ER-) were checked by RT-PCR (A) and relative band intensities were compared with each β-actin control (B). β-Actin was included as an internal control. For MCF-7 (ER+) cells, ICAM-1 mRNA level in the pc3-GD3s-transfected MCF-7 cells was examined by Western blot analysis (C) and relative band intensity was also compared with GAPDH control (D). All experiments performed at least three times. We examined mean differences between groups by using the error bar graph procedure.
Figure Legend Snippet: Differential regulation of ICAM-1 expression in pc3-GD3s-trasnfected SK-BR3 (ER-) and MCF-7 (ER+) cells. Expression levels of GM3 synthase, GD3 synthase and ICAM-1 mRNAs in the pc3-GD3s-transfected SK-BR3 (ER-) were checked by RT-PCR (A) and relative band intensities were compared with each β-actin control (B). β-Actin was included as an internal control. For MCF-7 (ER+) cells, ICAM-1 mRNA level in the pc3-GD3s-transfected MCF-7 cells was examined by Western blot analysis (C) and relative band intensity was also compared with GAPDH control (D). All experiments performed at least three times. We examined mean differences between groups by using the error bar graph procedure.

Techniques Used: Expressing, Transfection, Reverse Transcription Polymerase Chain Reaction, Western Blot

26) Product Images from "House Dust Mite Induces Expression of Intercellular Adhesion Molecule-1 in EoL-1 Human Eosinophilic Leukemic Cells"

Article Title: House Dust Mite Induces Expression of Intercellular Adhesion Molecule-1 in EoL-1 Human Eosinophilic Leukemic Cells

Journal: Journal of Korean Medical Science

doi: 10.3346/jkms.2007.22.5.815

Effect of various inhibitors of MAPKs on HDM extract-induced ICAM-1 expression on EoL-1 cells. Results are expressed as the mean±SEM from four different experiments. * , p
Figure Legend Snippet: Effect of various inhibitors of MAPKs on HDM extract-induced ICAM-1 expression on EoL-1 cells. Results are expressed as the mean±SEM from four different experiments. * , p

Techniques Used: Expressing

Effect of MG-132 on HDM extract-induced ICAM-1 expression on EoL-1 cells. Results are expressed as the mean±SEM from four different experiments. * , p
Figure Legend Snippet: Effect of MG-132 on HDM extract-induced ICAM-1 expression on EoL-1 cells. Results are expressed as the mean±SEM from four different experiments. * , p

Techniques Used: Expressing

Effect of TNF-α and HDM extract on the expression of cell surface ICAM-1 on EoL-1 cells. EoL-1 cells were incubated with or without HDM extract (5-200 µg/mL) for 4.5 hr. TNF-α (20 ng/mL) was used as a positive control. Data are expressed as the mean±SEM of triplicate experiments. * , p
Figure Legend Snippet: Effect of TNF-α and HDM extract on the expression of cell surface ICAM-1 on EoL-1 cells. EoL-1 cells were incubated with or without HDM extract (5-200 µg/mL) for 4.5 hr. TNF-α (20 ng/mL) was used as a positive control. Data are expressed as the mean±SEM of triplicate experiments. * , p

Techniques Used: Expressing, Incubation, Positive Control

27) Product Images from "Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats"

Article Title: Role of carbonyl sulfide in acute lung injury following limb ischemia/reperfusion in rats

Journal: European Journal of Medical Research

doi: 10.1186/s40001-017-0255-z

Effects of COS on ICAM-1 expression in the lung tissues. Results are given as mean ± SD ( n = 8 animals/group). Significant differences are indicated as: * p
Figure Legend Snippet: Effects of COS on ICAM-1 expression in the lung tissues. Results are given as mean ± SD ( n = 8 animals/group). Significant differences are indicated as: * p

Techniques Used: Expressing

28) Product Images from "Dendritic Cell-Mediated Viral Transfer to T Cells Is Required for Human Immunodeficiency Virus Type 1 Persistence in the Face of Rapid Cell Turnover"

Article Title: Dendritic Cell-Mediated Viral Transfer to T Cells Is Required for Human Immunodeficiency Virus Type 1 Persistence in the Face of Rapid Cell Turnover

Journal: Journal of Virology

doi: 10.1128/JVI.76.21.10692-10701.2002

Cell-to-cell adhesion is required for optimal virus transfer. THP1-DC-SIGN cells (A) or DC (B) (2 × 10 4 cells each) were incubated with HIV Lai for 2 h at 37°C, washed, and cocultured with activated T cells (2 × 10 5 cells) in the presence of blocking antibodies against LFA-3 (20 μg/ml), LFA-1 (20 μg/ml), ICAM-1 (20 μg/ml), a combination of all three antibodies (each at 10 μg/ml), or isotype-matched control antibody. Antibodies were added to T cells prior to their coculture with HIV-pulsed DC or THP1-DC-SIGN cells. As controls, THP1-DC-SIGN cells, DC, or activated T cells were incubated with HIV Lai , washed, and then cultured alone (cell-free infection). Supernatants were collected 2 days after the initiation of the coculture and assayed for the p24 gag content by ELISA. The p24 gag values represent means ± standard deviations (error bars) of triplicate cultures. One representative experiment out of two is shown.
Figure Legend Snippet: Cell-to-cell adhesion is required for optimal virus transfer. THP1-DC-SIGN cells (A) or DC (B) (2 × 10 4 cells each) were incubated with HIV Lai for 2 h at 37°C, washed, and cocultured with activated T cells (2 × 10 5 cells) in the presence of blocking antibodies against LFA-3 (20 μg/ml), LFA-1 (20 μg/ml), ICAM-1 (20 μg/ml), a combination of all three antibodies (each at 10 μg/ml), or isotype-matched control antibody. Antibodies were added to T cells prior to their coculture with HIV-pulsed DC or THP1-DC-SIGN cells. As controls, THP1-DC-SIGN cells, DC, or activated T cells were incubated with HIV Lai , washed, and then cultured alone (cell-free infection). Supernatants were collected 2 days after the initiation of the coculture and assayed for the p24 gag content by ELISA. The p24 gag values represent means ± standard deviations (error bars) of triplicate cultures. One representative experiment out of two is shown.

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

29) Product Images from "CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis"

Article Title: CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis

Journal: PLoS ONE

doi: 10.1371/journal.pone.0182643

CX3CR1 -/- enhances left ventricular expression of adhesion molecules and pro-inflammatory cytokines in Coxsackievirus B3-infected mice. Induction of ICAM-1 (A) and VCAM-1 (B) as well as of pro-inflammatory cytokines (C-F) in CX3CR1 -/- mice compared to WT CVB3 mice. The quantitative determination of ICAM-1 and VCAM-1, indicated by the positive area (%) in relation to the heart area (mm 2 ), was performed via digital image analysis at a 200x magnification (scale bar = 200 μm). Bar graphs represent the mean ± SEM. Statistical analysis was performed by One-way ANOVA or the Kruskal-Wallis test. *p
Figure Legend Snippet: CX3CR1 -/- enhances left ventricular expression of adhesion molecules and pro-inflammatory cytokines in Coxsackievirus B3-infected mice. Induction of ICAM-1 (A) and VCAM-1 (B) as well as of pro-inflammatory cytokines (C-F) in CX3CR1 -/- mice compared to WT CVB3 mice. The quantitative determination of ICAM-1 and VCAM-1, indicated by the positive area (%) in relation to the heart area (mm 2 ), was performed via digital image analysis at a 200x magnification (scale bar = 200 μm). Bar graphs represent the mean ± SEM. Statistical analysis was performed by One-way ANOVA or the Kruskal-Wallis test. *p

Techniques Used: Expressing, Infection, Mouse Assay

30) Product Images from "Ursolic acid, a natural pentacyclic triterpenoid, inhibits intracellular trafficking of proteins and induces accumulation of intercellular adhesion molecule-1 linked to high-mannose-type glycans in the endoplasmic reticulum"

Article Title: Ursolic acid, a natural pentacyclic triterpenoid, inhibits intracellular trafficking of proteins and induces accumulation of intercellular adhesion molecule-1 linked to high-mannose-type glycans in the endoplasmic reticulum

Journal: FEBS Open Bio

doi: 10.1016/j.fob.2014.02.009

Brefeldin A, but not 1-deoxymannojirimycin, inhibits IL-1α-induced cell-surface ICAM-1 expression. A549 cells were preincubated with various concentrations of 1-deoxymannojirimycin (A) or brefeldin A (B) for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P
Figure Legend Snippet: Brefeldin A, but not 1-deoxymannojirimycin, inhibits IL-1α-induced cell-surface ICAM-1 expression. A549 cells were preincubated with various concentrations of 1-deoxymannojirimycin (A) or brefeldin A (B) for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P

Techniques Used: Expressing, Incubation, Enzyme-linked Immunosorbent Assay

Ursolic acid inhibits IL-1α-induced cell-surface ICAM-1 expression. (A–C) A549 cells (A), MCF-7 cells (B), and HUVEC (C) were preincubated with various concentrations of ursolic acid for 1 h and then incubated with (filled circles) or without (open circles) IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P
Figure Legend Snippet: Ursolic acid inhibits IL-1α-induced cell-surface ICAM-1 expression. (A–C) A549 cells (A), MCF-7 cells (B), and HUVEC (C) were preincubated with various concentrations of ursolic acid for 1 h and then incubated with (filled circles) or without (open circles) IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P

Techniques Used: Expressing, Incubation, Enzyme-linked Immunosorbent Assay

Ursolic acid affects N-linked oligosaccharide processing of ICAM-1. (A) A549 cells were treated with various concentrations of tunicamycin for 1 h and then incubated with (+) or without (−) IL-1α (0.25 ng/ml) for 6 h. Cell lysates were analyzed by Western blotting. Data are representative of three independent experiments. (B) A549 cells were preincubated with various concentrations of tunicamycin for 1 h and then incubated with (filled circles) or without (open circles) IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P
Figure Legend Snippet: Ursolic acid affects N-linked oligosaccharide processing of ICAM-1. (A) A549 cells were treated with various concentrations of tunicamycin for 1 h and then incubated with (+) or without (−) IL-1α (0.25 ng/ml) for 6 h. Cell lysates were analyzed by Western blotting. Data are representative of three independent experiments. (B) A549 cells were preincubated with various concentrations of tunicamycin for 1 h and then incubated with (filled circles) or without (open circles) IL-1α (0.25 ng/ml) for 6 h. Cell-surface ICAM-1 expression was measured by the Cell-ELISA assay. ICAM-1 expression (%) is represented by the means ± S.D. of triplicate cultures. ∗∗ P

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

Ursolic acid does not inhibit IL-1α-induced expression of ICAM-1 at the protein level but affects its post-translational modification. A549 cells (A), MCF-7 cells (B), and HUVEC (C) were preincubated with various concentrations of ursolic acid for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h. Cell lysates were analyzed by Western blotting. Data are representative of at least three independent experiments for A549 cells and MCF-7 cells and two independent experiments for HUVEC.
Figure Legend Snippet: Ursolic acid does not inhibit IL-1α-induced expression of ICAM-1 at the protein level but affects its post-translational modification. A549 cells (A), MCF-7 cells (B), and HUVEC (C) were preincubated with various concentrations of ursolic acid for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h. Cell lysates were analyzed by Western blotting. Data are representative of at least three independent experiments for A549 cells and MCF-7 cells and two independent experiments for HUVEC.

Techniques Used: Expressing, Modification, Incubation, Western Blot

Ursolic acid induces accumulation of ICAM-1 in ER. A549 cells were preincubated with or without ursolic acid (50 μM) for 1 h and then incubated with or without IL-1α (0.25 ng/ml) for 6 h in the presence or absence of ursolic acid. Cells were fixed and stained for ICAM-1 (green), together with GM130 (red) (A) and calnexin (red) (B) as markers of Golgi apparatus and ER, respectively. Panels A and B show higher magnification images of representative cells in Figs. S3 and S4 , respectively. Scale bars represent 20 μm. Data are representative of at least three independent experiments. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
Figure Legend Snippet: Ursolic acid induces accumulation of ICAM-1 in ER. A549 cells were preincubated with or without ursolic acid (50 μM) for 1 h and then incubated with or without IL-1α (0.25 ng/ml) for 6 h in the presence or absence of ursolic acid. Cells were fixed and stained for ICAM-1 (green), together with GM130 (red) (A) and calnexin (red) (B) as markers of Golgi apparatus and ER, respectively. Panels A and B show higher magnification images of representative cells in Figs. S3 and S4 , respectively. Scale bars represent 20 μm. Data are representative of at least three independent experiments. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Techniques Used: Incubation, Staining

Ursolic acid inhibits intracellular protein transport from ER to Golgi apparatus in a manner distinct from brefeldin A. A549 cells were preincubated with or without ursolic acid (50 μM), brefeldin A (100 nM) or 1-deoxymannojirimycin (100 μM) for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h in the presence or absence of the compounds. Cells were fixed and stained for ICAM-1 (green), together with GM130 (red) (A) and calnexin (red) (B) as markers of Golgi apparatus and ER, respectively. Panels A and B show higher magnification images of representative cells in Figs. S5 and S6 , respectively. Scale bars represent 20 μm. Data are representative of at least three independent experiments. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
Figure Legend Snippet: Ursolic acid inhibits intracellular protein transport from ER to Golgi apparatus in a manner distinct from brefeldin A. A549 cells were preincubated with or without ursolic acid (50 μM), brefeldin A (100 nM) or 1-deoxymannojirimycin (100 μM) for 1 h and then incubated with IL-1α (0.25 ng/ml) for 6 h in the presence or absence of the compounds. Cells were fixed and stained for ICAM-1 (green), together with GM130 (red) (A) and calnexin (red) (B) as markers of Golgi apparatus and ER, respectively. Panels A and B show higher magnification images of representative cells in Figs. S5 and S6 , respectively. Scale bars represent 20 μm. Data are representative of at least three independent experiments. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Techniques Used: Incubation, Staining

31) Product Images from "Tethering of ICAM on target cells is required for LFA-1-dependent NK cell adhesion and granule polarization"

Article Title: Tethering of ICAM on target cells is required for LFA-1-dependent NK cell adhesion and granule polarization

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

doi: 10.4049/jimmunol.1000761

Disruption of actin filaments in target cells increases ICAM-1 mobility. ICAM-1 mobility was determined by Fluorescence Recovery after Photobleaching (FRAP). Cells were stained with a PE-labeled anti-ICAM-1 antibody. Fluorescence recovery in the bleached
Figure Legend Snippet: Disruption of actin filaments in target cells increases ICAM-1 mobility. ICAM-1 mobility was determined by Fluorescence Recovery after Photobleaching (FRAP). Cells were stained with a PE-labeled anti-ICAM-1 antibody. Fluorescence recovery in the bleached

Techniques Used: Fluorescence, Staining, Labeling

Movement of human resting NK cells over mobile and immobile ICAM-1. NK cells were visualized 20 minutes after injection into chambers containing ICAM-1 bound to either lipid bilayers or glass surfaces, respectively. The movement of NK cells was tracked
Figure Legend Snippet: Movement of human resting NK cells over mobile and immobile ICAM-1. NK cells were visualized 20 minutes after injection into chambers containing ICAM-1 bound to either lipid bilayers or glass surfaces, respectively. The movement of NK cells was tracked

Techniques Used: Injection

Disruption of actin filaments increases the mobility of ICAM-1 and ICAM-2. The mobility of ICAM-1 ( A , upper panel, bar indicates 5 μm, B and D , left side) and ICAM-2 ( A , lower panel, B and D , right side) in 721.221 cells treated with the indicated
Figure Legend Snippet: Disruption of actin filaments increases the mobility of ICAM-1 and ICAM-2. The mobility of ICAM-1 ( A , upper panel, bar indicates 5 μm, B and D , left side) and ICAM-2 ( A , lower panel, B and D , right side) in 721.221 cells treated with the indicated

Techniques Used:

Disruption of actin filaments increases the mobility of ICAM-1 on K562 cells and decreases conjugate formation with NK cells. The mobility of ICAM-1 was determined by FRAP. Cells were stained with a PE-labeled anti-ICAM-1 antibody. Fluorescence recovery
Figure Legend Snippet: Disruption of actin filaments increases the mobility of ICAM-1 on K562 cells and decreases conjugate formation with NK cells. The mobility of ICAM-1 was determined by FRAP. Cells were stained with a PE-labeled anti-ICAM-1 antibody. Fluorescence recovery

Techniques Used: Staining, Labeling, Fluorescence

32) Product Images from "Arachidonic Acid but not Eicosapentaenoic Acid (EPA) and Oleic Acid Activates NF-?B and Elevates ICAM-1 Expression in Caco-2 Cells "

Article Title: Arachidonic Acid but not Eicosapentaenoic Acid (EPA) and Oleic Acid Activates NF-?B and Elevates ICAM-1 Expression in Caco-2 Cells

Journal: Lipids

doi: 10.1007/s11745-007-3071-3

a, b ICAM-1 expression (in arbitrary units a.u.) on living control Caco-2 cells and after pre-treatment with PPAR agonists (2 h; PPARγ troglitazone 100 μM and PPARα GW7647 1 μM) and c, d NF-κB transactivation measured by luciferase activity (in RLU/mg) in a NF-κB reporter Caco-2 cell-line of control cells and after troglitazone pre-treatment with and without cytokine stimulation for 3 h (100 U/mL IFNγ and 50 U/mL IL-1β) and net stimulated (stimulated–non-stimulated). Results represent means ± SD; n = 2. Representative representation of two independent experiments. b P
Figure Legend Snippet: a, b ICAM-1 expression (in arbitrary units a.u.) on living control Caco-2 cells and after pre-treatment with PPAR agonists (2 h; PPARγ troglitazone 100 μM and PPARα GW7647 1 μM) and c, d NF-κB transactivation measured by luciferase activity (in RLU/mg) in a NF-κB reporter Caco-2 cell-line of control cells and after troglitazone pre-treatment with and without cytokine stimulation for 3 h (100 U/mL IFNγ and 50 U/mL IL-1β) and net stimulated (stimulated–non-stimulated). Results represent means ± SD; n = 2. Representative representation of two independent experiments. b P

Techniques Used: Expressing, Luciferase, Activity Assay

a – b ICAM-1 expression (in arbitrary units a.u.) on living Caco-2 cells cultured for 22 days with 160 μM oleic acid (OA) or 130 μM arachidonic acid (ARA) plus 30 μM OA or 6 μM eicosapentaenoic acid (EPA) plus 154 μM OA with and without cytokine stimulation for 16 h (100 U/mL IFNγ and 50 U/mL IL-1β) and net stimulated (stimulated–non-stimulated). Results represent means ± SD; n = 2. Representative representation of two independent experiments. ANOVA between groups, non-stimulated P
Figure Legend Snippet: a – b ICAM-1 expression (in arbitrary units a.u.) on living Caco-2 cells cultured for 22 days with 160 μM oleic acid (OA) or 130 μM arachidonic acid (ARA) plus 30 μM OA or 6 μM eicosapentaenoic acid (EPA) plus 154 μM OA with and without cytokine stimulation for 16 h (100 U/mL IFNγ and 50 U/mL IL-1β) and net stimulated (stimulated–non-stimulated). Results represent means ± SD; n = 2. Representative representation of two independent experiments. ANOVA between groups, non-stimulated P

Techniques Used: Expressing, Cell Culture, Acetylene Reduction Assay

Model validation. a ICAM-1 expression (in arbitrary units a.u.) on living control Caco-2 cells and after 2 h pre-treatment with 1 μM dexamethasone or 30 min 5 mM sulfasalazine with and without cytokine stimulation for 16 h (100 U/mL IFNγ and 50 U/mL IL-1β) and b net stimulated (stimulated–non-stimulated) ICAM-1 expression. Results represent means ± SD; n = 2. Representative representation of two independent experiments. a P
Figure Legend Snippet: Model validation. a ICAM-1 expression (in arbitrary units a.u.) on living control Caco-2 cells and after 2 h pre-treatment with 1 μM dexamethasone or 30 min 5 mM sulfasalazine with and without cytokine stimulation for 16 h (100 U/mL IFNγ and 50 U/mL IL-1β) and b net stimulated (stimulated–non-stimulated) ICAM-1 expression. Results represent means ± SD; n = 2. Representative representation of two independent experiments. a P

Techniques Used: Expressing

33) Product Images from "Self-medication by orang-utans (Pongo pygmaeus) using bioactive properties of Dracaena cantleyi"

Article Title: Self-medication by orang-utans (Pongo pygmaeus) using bioactive properties of Dracaena cantleyi

Journal: Scientific Reports

doi: 10.1038/s41598-017-16621-w

ICAM-1 ELISA: HUVECs were treated with 10, 20 and 30 µg/ml of extracts for 30 min followed by TNFα for 24 h and ICAM-1 determined by sandwich ELISA.
Figure Legend Snippet: ICAM-1 ELISA: HUVECs were treated with 10, 20 and 30 µg/ml of extracts for 30 min followed by TNFα for 24 h and ICAM-1 determined by sandwich ELISA.

Techniques Used: Enzyme-linked Immunosorbent Assay, Sandwich ELISA

34) Product Images from "Promotion of a cancer-like phenotype, through chronic exposure to inflammatory cytokines and hypoxia in a bronchial epithelial cell line model"

Article Title: Promotion of a cancer-like phenotype, through chronic exposure to inflammatory cytokines and hypoxia in a bronchial epithelial cell line model

Journal: Scientific Reports

doi: 10.1038/srep18907

Adhesion molecule expression is altered due to chromic inflammatory and hypoxia exposure. Cell surface staining of ( a ) ICAM-1, ( b ) VCAM-1 by FACS on (i) HBEC4 ctl, (ii) EVC clones, (iii) normoxia clones and (iv) hypoxia clones and representative flow cytometry plots for ( c ) Normoxia and ( d ) Hypoxia. Cells were continuously cultured for a period of three months. Values based on a dot blot analysis using percentage-gated values. Isogenic controls were used for each individual sample and this value was subtracted from each sample value. (20,000 events counted, n = 1).
Figure Legend Snippet: Adhesion molecule expression is altered due to chromic inflammatory and hypoxia exposure. Cell surface staining of ( a ) ICAM-1, ( b ) VCAM-1 by FACS on (i) HBEC4 ctl, (ii) EVC clones, (iii) normoxia clones and (iv) hypoxia clones and representative flow cytometry plots for ( c ) Normoxia and ( d ) Hypoxia. Cells were continuously cultured for a period of three months. Values based on a dot blot analysis using percentage-gated values. Isogenic controls were used for each individual sample and this value was subtracted from each sample value. (20,000 events counted, n = 1).

Techniques Used: Expressing, Staining, FACS, CTL Assay, Clone Assay, Flow Cytometry, Cytometry, Cell Culture, Dot Blot

35) Product Images from "KCa1.1 and Kv1.3 channels regulate the interactions between fibroblast-like synoviocytes and T lymphocytes during rheumatoid arthritis"

Article Title: KCa1.1 and Kv1.3 channels regulate the interactions between fibroblast-like synoviocytes and T lymphocytes during rheumatoid arthritis

Journal: Arthritis Research & Therapy

doi: 10.1186/s13075-018-1783-9

Collagen-induced arthritis fibroblast-like synoviocytes (CIA-FLS) express major histocompatibility complex (MHC) class II molecules that are regulated through KCa1.1, as well as antigen-presenting proteins . a CIA-FLS plasma membrane expression of MHC class II protein following stimulation for 72 h with IFN-γ ( gray circles ), paxilline (Pax; black squares ), or interferon (IFN)-γ and paxilline ( open squares ). Data are presented as mean ± SEM ( n = 3–8 CIA-FLS donors). b Flow cytometric histogram of CIA-FLS stained for the plasma membrane expression of MHC class II protein in cells treated with paxilline for 72 h ( dashed line ), stimulated for 72 h with IFN-γ ( solid line ), or stimulated for 72 h with IFN-γ and paxilline ( dotted line ). The shaded histogram represents background staining. c MHC class II molecule expression of CIA-FLS that were permeabilized with saponin prior to staining for MHC class II in cells treated for 72 h with IFN-γ ( gray circles ), paxilline ( black squares ), or IFN-γ and paxilline ( open squares ). Data are presented as mean ± SEM ( n = 3–6 CIA-FLS donors). d Flow cytometric histogram of CIA-FLS stained for MHC class II molecules following permeabilization with saponin in cells treated for 72 h with IFN-γ ( solid line ), paxilline ( dashed line ), or IFN-γ and paxilline ( dotted line ). The shaded histogram represents background staining. e Expression of intercellular adhesion molecule (ICAM)-1, B7-H3, and CD40 by CIA-FLS following treatment for 72 h with IFN-γ, paxilline, or IFN-γ and paxilline. Data are presented as mean ± SEM ( n = 6 CIA-FLS donors). * p
Figure Legend Snippet: Collagen-induced arthritis fibroblast-like synoviocytes (CIA-FLS) express major histocompatibility complex (MHC) class II molecules that are regulated through KCa1.1, as well as antigen-presenting proteins . a CIA-FLS plasma membrane expression of MHC class II protein following stimulation for 72 h with IFN-γ ( gray circles ), paxilline (Pax; black squares ), or interferon (IFN)-γ and paxilline ( open squares ). Data are presented as mean ± SEM ( n = 3–8 CIA-FLS donors). b Flow cytometric histogram of CIA-FLS stained for the plasma membrane expression of MHC class II protein in cells treated with paxilline for 72 h ( dashed line ), stimulated for 72 h with IFN-γ ( solid line ), or stimulated for 72 h with IFN-γ and paxilline ( dotted line ). The shaded histogram represents background staining. c MHC class II molecule expression of CIA-FLS that were permeabilized with saponin prior to staining for MHC class II in cells treated for 72 h with IFN-γ ( gray circles ), paxilline ( black squares ), or IFN-γ and paxilline ( open squares ). Data are presented as mean ± SEM ( n = 3–6 CIA-FLS donors). d Flow cytometric histogram of CIA-FLS stained for MHC class II molecules following permeabilization with saponin in cells treated for 72 h with IFN-γ ( solid line ), paxilline ( dashed line ), or IFN-γ and paxilline ( dotted line ). The shaded histogram represents background staining. e Expression of intercellular adhesion molecule (ICAM)-1, B7-H3, and CD40 by CIA-FLS following treatment for 72 h with IFN-γ, paxilline, or IFN-γ and paxilline. Data are presented as mean ± SEM ( n = 6 CIA-FLS donors). * p

Techniques Used: Expressing, Flow Cytometry, Staining

36) Product Images from "Phenotypic and Functional Changes in Blood Monocytes Following Adherence to Endothelium"

Article Title: Phenotypic and Functional Changes in Blood Monocytes Following Adherence to Endothelium

Journal: PLoS ONE

doi: 10.1371/journal.pone.0037091

Increased expression of VEGFR2 and VCAM-1, reduced expression of CD36 and expression of CD31 and ICAM-1 in the endothelium-adherent monocytes in co-culture. HLA-A2+ PBMCs (1×10 6 cells/well) were incubated for 2 h (Day 0) with HLA-A2− HUVEC, after which the non-adherent cells were removed by washing. The cell layers were analysed by dual-colour flow cytometry for HLA-A2 and VEGFR2 expression on Day 1 (A) and Day 2 (B) of co-culture, VCAM-1 expression in the absence of TNF-α on Day 6 of co-culture (C), VCAM-1 expression on Day 6 of co-culture after 24 hours of stimulation with TNF-α (10 ng/ml) (D), CD36 expression on Day 0 (E) and Day 1 (F) of co-culture, as well as CD31 (G) and ICAM-1 (H) expression on Day 0. Representative plots from 2–5 individual experiments are shown.
Figure Legend Snippet: Increased expression of VEGFR2 and VCAM-1, reduced expression of CD36 and expression of CD31 and ICAM-1 in the endothelium-adherent monocytes in co-culture. HLA-A2+ PBMCs (1×10 6 cells/well) were incubated for 2 h (Day 0) with HLA-A2− HUVEC, after which the non-adherent cells were removed by washing. The cell layers were analysed by dual-colour flow cytometry for HLA-A2 and VEGFR2 expression on Day 1 (A) and Day 2 (B) of co-culture, VCAM-1 expression in the absence of TNF-α on Day 6 of co-culture (C), VCAM-1 expression on Day 6 of co-culture after 24 hours of stimulation with TNF-α (10 ng/ml) (D), CD36 expression on Day 0 (E) and Day 1 (F) of co-culture, as well as CD31 (G) and ICAM-1 (H) expression on Day 0. Representative plots from 2–5 individual experiments are shown.

Techniques Used: Expressing, Co-Culture Assay, Incubation, Flow Cytometry, Cytometry

37) Product Images from "The p55TNFR-IKK2-Ripk3 axis orchestrates arthritis by regulating death and inflammatory pathways in synovial fibroblasts"

Article Title: The p55TNFR-IKK2-Ripk3 axis orchestrates arthritis by regulating death and inflammatory pathways in synovial fibroblasts

Journal: Nature Communications

doi: 10.1038/s41467-018-02935-4

IKK2 deficiency differentially affects gene expression of naive and arthritic SFs. a Representative immunodetection of IKK2 levels in TAT-Cre treated Ikk2 f/f ( Ikk2 Δ/Δ ) and TAT-Cre treated hTNFtg Ikk2 f/f ( hTNFtg Ikk2 Δ/Δ ) SFs compared to non-treated control cultures Ikk2 f/f and hTNFtg Ikk2 f/f , respectively (upper panel). b Representative MTT incorporation assay in the indicated genotypes; hTNF quantitation in the supernatants of hTNFtg Ikk2 Δ/Δ (grey column) and control hTNFtg Ikk2 f/f SF cultures (black column) ( n = 7, 2 experiments); flow cytometric detection of Vcam-1 and Icam-1 levels in cultured hTNFtg Ikk2 f/f (black), hTNFtg Ikk2 Δ/Δ (grey) and control SFs ( Ikk2 f/f : dotted black and Ikk2 Δ/Δ : dotted grey) ( n = 4, 2 experiments). c Representative immunodetection of Casp8 (C8), Cleaved Casp3 (CC3), Parp1, Sod2, Xiap, cIAP-1 and cFLIP (L) in cell extracts of Ikk2 Δ/Δ , hTNFtg Ikk2 Δ/Δ and control SF cultures treated with TNF (20 ng/ml, 5 h) ( n = 10). d Relative gene expression of the NFκB-regulated genes Il6 , Mmp-3 , -13 , -14 , Timp1 , Il1b and Tnfsf11 (RankL) (normalized to b2m levels) in SFs of the indicated genotypes upon TNF (20 ng/ml, 5 h) ( n = 3–8). e Survival rates of Ikk2 Δ/Δ and hTNFtg Ikk2 Δ/Δ SFs treated with TNF, zVAD, Nec1s and GW806742X (GW) as indicated ( n = 3). f Representative immunodetection of pMlkl, Mlkl, Ripk3, cFLIP (S) and IKK2 levels in TNF-treated Ikk2 Δ/Δ , hTNFtg Ikk2 Δ/Δ and control SF cultures (TNF: 20 ng/ml, 5 h) ( n = 8, 4 experiments). Data are presented as the mean ± SEM. * P
Figure Legend Snippet: IKK2 deficiency differentially affects gene expression of naive and arthritic SFs. a Representative immunodetection of IKK2 levels in TAT-Cre treated Ikk2 f/f ( Ikk2 Δ/Δ ) and TAT-Cre treated hTNFtg Ikk2 f/f ( hTNFtg Ikk2 Δ/Δ ) SFs compared to non-treated control cultures Ikk2 f/f and hTNFtg Ikk2 f/f , respectively (upper panel). b Representative MTT incorporation assay in the indicated genotypes; hTNF quantitation in the supernatants of hTNFtg Ikk2 Δ/Δ (grey column) and control hTNFtg Ikk2 f/f SF cultures (black column) ( n = 7, 2 experiments); flow cytometric detection of Vcam-1 and Icam-1 levels in cultured hTNFtg Ikk2 f/f (black), hTNFtg Ikk2 Δ/Δ (grey) and control SFs ( Ikk2 f/f : dotted black and Ikk2 Δ/Δ : dotted grey) ( n = 4, 2 experiments). c Representative immunodetection of Casp8 (C8), Cleaved Casp3 (CC3), Parp1, Sod2, Xiap, cIAP-1 and cFLIP (L) in cell extracts of Ikk2 Δ/Δ , hTNFtg Ikk2 Δ/Δ and control SF cultures treated with TNF (20 ng/ml, 5 h) ( n = 10). d Relative gene expression of the NFκB-regulated genes Il6 , Mmp-3 , -13 , -14 , Timp1 , Il1b and Tnfsf11 (RankL) (normalized to b2m levels) in SFs of the indicated genotypes upon TNF (20 ng/ml, 5 h) ( n = 3–8). e Survival rates of Ikk2 Δ/Δ and hTNFtg Ikk2 Δ/Δ SFs treated with TNF, zVAD, Nec1s and GW806742X (GW) as indicated ( n = 3). f Representative immunodetection of pMlkl, Mlkl, Ripk3, cFLIP (S) and IKK2 levels in TNF-treated Ikk2 Δ/Δ , hTNFtg Ikk2 Δ/Δ and control SF cultures (TNF: 20 ng/ml, 5 h) ( n = 8, 4 experiments). Data are presented as the mean ± SEM. * P

Techniques Used: Expressing, Immunodetection, MTT Assay, Quantitation Assay, Flow Cytometry, Cell Culture

38) Product Images from "Phase I Study of a Poxviral TRICOM-Based Vaccine Directed Against the Transcription Factor Brachyury"

Article Title: Phase I Study of a Poxviral TRICOM-Based Vaccine Directed Against the Transcription Factor Brachyury

Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

doi: 10.1158/1078-0432.CCR-17-1087

(A) Flow cytometric analysis of CD80 (B7.1), CD54 (ICAM-1), and CD58 (LFA-3) expression in human DCs infected with indicated vectors (10 MOI, 24-hour). Shown is the percent positive cells for each marker and the mean fluorescence intensity (MFI). (B) Western blot analysis of brachyury expression in protein lysates of indicated DC cultures. GAPDH is used as a loading control protein for each sample. (C) Immunofluorescence analysis of brachyury expression in indicated DC cultures; green corresponds to brachyury and blue corresponds to DAPI-stained nuclei. Magnification 20X.
Figure Legend Snippet: (A) Flow cytometric analysis of CD80 (B7.1), CD54 (ICAM-1), and CD58 (LFA-3) expression in human DCs infected with indicated vectors (10 MOI, 24-hour). Shown is the percent positive cells for each marker and the mean fluorescence intensity (MFI). (B) Western blot analysis of brachyury expression in protein lysates of indicated DC cultures. GAPDH is used as a loading control protein for each sample. (C) Immunofluorescence analysis of brachyury expression in indicated DC cultures; green corresponds to brachyury and blue corresponds to DAPI-stained nuclei. Magnification 20X.

Techniques Used: Flow Cytometry, Expressing, Infection, Marker, Fluorescence, Western Blot, Immunofluorescence, Staining

39) Product Images from "Vitamin E down-modulates mitogen-activated protein kinases, nuclear factor-?B and inflammatory responses in lung epithelial cells"

Article Title: Vitamin E down-modulates mitogen-activated protein kinases, nuclear factor-?B and inflammatory responses in lung epithelial cells

Journal: Clinical and Experimental Immunology

doi: 10.1111/j.1365-2249.2006.03285.x

Effects of extracellular signal-regulated kinase (ERK)1/2 (PD98059), p38 (SP203580) and protein kinase C (PKC) (Calphostin C) inhibitors on tumour necrosis factor (TNF)-α-induced cell surface expression of intercellular adhesion molecule-1 (ICAM-1) on bronchial epithelial cell line (BEAS)-2B and A549 cells. Cells were preincubated with 40 µM PD98059, 1 µM SB203580 or 0·5 µM Calphostin C. For comparison, treatment with 50 µM α-tocopherol was included in the experiment. The surface expression of ICAM-1 was measured by flow cytometry. Results are expressed as percentage of remaining cell surface expression of ICAM-1 versus TNF-α-stimulated cells. Expression on cells stimulated with TNF-α alone was given the value 100%. Statistical comparisons were performed using one-sample t -test versus 100% ( n = 4).
Figure Legend Snippet: Effects of extracellular signal-regulated kinase (ERK)1/2 (PD98059), p38 (SP203580) and protein kinase C (PKC) (Calphostin C) inhibitors on tumour necrosis factor (TNF)-α-induced cell surface expression of intercellular adhesion molecule-1 (ICAM-1) on bronchial epithelial cell line (BEAS)-2B and A549 cells. Cells were preincubated with 40 µM PD98059, 1 µM SB203580 or 0·5 µM Calphostin C. For comparison, treatment with 50 µM α-tocopherol was included in the experiment. The surface expression of ICAM-1 was measured by flow cytometry. Results are expressed as percentage of remaining cell surface expression of ICAM-1 versus TNF-α-stimulated cells. Expression on cells stimulated with TNF-α alone was given the value 100%. Statistical comparisons were performed using one-sample t -test versus 100% ( n = 4).

Techniques Used: Expressing, Flow Cytometry, Cytometry

Effect of α-tocopherol on monocyte adherence to tumour necrosis factor (TNF)-α-activated bronchial epithelial cell line (BEAS)-2B cells.  51 Cr-labelled U937 cells were added to BEAS-2B monolayer treated with α-tocopherol in a concentration range of 25–100 µM followed by stimulation with 10 ng/ml TNF-α for 20 h. After 45 min non-adherent cells were removed by washing and remaining cells were lysed with 5% Triton. The lysates were assayed for  51 Cr activity. Data are presented as fold increase of adhesion  versus  unstimulated cells. For comparison, the effect of pretreatment with antibodies against intercellular adhesion molecule-1 (α-ICAM) and vascular cell adhesion molecule-1 (α-VCAM) is also shown. Statistical significance  versus  cells stimulated with TNF-α alone is indicated (analysis of variance and Dunnet's multiple comparison test,  n  = 6).
Figure Legend Snippet: Effect of α-tocopherol on monocyte adherence to tumour necrosis factor (TNF)-α-activated bronchial epithelial cell line (BEAS)-2B cells. 51 Cr-labelled U937 cells were added to BEAS-2B monolayer treated with α-tocopherol in a concentration range of 25–100 µM followed by stimulation with 10 ng/ml TNF-α for 20 h. After 45 min non-adherent cells were removed by washing and remaining cells were lysed with 5% Triton. The lysates were assayed for 51 Cr activity. Data are presented as fold increase of adhesion versus unstimulated cells. For comparison, the effect of pretreatment with antibodies against intercellular adhesion molecule-1 (α-ICAM) and vascular cell adhesion molecule-1 (α-VCAM) is also shown. Statistical significance versus cells stimulated with TNF-α alone is indicated (analysis of variance and Dunnet's multiple comparison test, n = 6).

Techniques Used: Concentration Assay, Activity Assay

Effect of α-tocopherol on cell surface expression of adhesion molecules intercellular adhesion molecule-1 (ICAM-1) on bronchial epithelial cell line (BEAS)-2B (a), normal human bronchial epithelial cells (NHBE) (b), A549 (c) and vascular cell adhesion molecule (VCAM)-1 on BEAS-2B (d) cells. Cells were treated for 45 min with α-tocopherol in a concentration range of 25–100 µM and thereafter stimulated for 20 h with 10 ng/ml tumour necrosis factor (TNF)-α. The surface expression of ICAM-1 and VCAM-1 was measured by flow cytometry. Data are presented as fold increase of median fluorescence of ICAM-1 or VCAM-1 expression versus unstimulated cells. Statistical significance versus cells stimulated with TNF-α alone is indicated (analysis of variance and Dunnet's multiple comparison test). n = 4 except for cells stimulated with TNF-α alone and α-tocopherol 50 in (a) and (c) ( n = 8).
Figure Legend Snippet: Effect of α-tocopherol on cell surface expression of adhesion molecules intercellular adhesion molecule-1 (ICAM-1) on bronchial epithelial cell line (BEAS)-2B (a), normal human bronchial epithelial cells (NHBE) (b), A549 (c) and vascular cell adhesion molecule (VCAM)-1 on BEAS-2B (d) cells. Cells were treated for 45 min with α-tocopherol in a concentration range of 25–100 µM and thereafter stimulated for 20 h with 10 ng/ml tumour necrosis factor (TNF)-α. The surface expression of ICAM-1 and VCAM-1 was measured by flow cytometry. Data are presented as fold increase of median fluorescence of ICAM-1 or VCAM-1 expression versus unstimulated cells. Statistical significance versus cells stimulated with TNF-α alone is indicated (analysis of variance and Dunnet's multiple comparison test). n = 4 except for cells stimulated with TNF-α alone and α-tocopherol 50 in (a) and (c) ( n = 8).

Techniques Used: Expressing, Concentration Assay, Flow Cytometry, Cytometry, Fluorescence

40) Product Images from "Azelnidipine Inhibits the Differentiation and Activation of THP-1 Macrophages through the L-Type Calcium Channel"

Article Title: Azelnidipine Inhibits the Differentiation and Activation of THP-1 Macrophages through the L-Type Calcium Channel

Journal: Journal of Atherosclerosis and Thrombosis

doi: 10.5551/jat.41798

Expressions of (A) ICAM-1 or (B) LOX-1 in THP-1 cells were measured by flow cytometry. * p
Figure Legend Snippet: Expressions of (A) ICAM-1 or (B) LOX-1 in THP-1 cells were measured by flow cytometry. * p

Techniques Used: Flow Cytometry, Cytometry

Related Articles

Functional Assay:

Article Title: High-Multiplicity HIV-1 Infection and Neutralizing Antibody Evasion Mediated by the Macrophage-T Cell Virological Synapse
Article Snippet: .. For functional assays, blocking antibodies all were purified mouse IgG1 used at 10 μg/ml unless otherwise stated: CD4 (13B.8.2; Beckman-Coulter), CCR5 (2D7; BD Biosciences), ICAM-1 (LB-2 IgG2b ; BD Biosciences or Santa-Cruz), LFA-1 (L130; BD Biosciences), ICAM-2 (B-T1; AbD Serotec), and ICAM-3 (101-1D2; Santa-Cruz). .. For laser scanning confocal microscopy (LSCM), we used the following primary MAb: CD4 (nonblocking; clone L120; mouse IgG1; CFAR), CD81 (clone 454720; mouse IgG2b ; R & D Systems), anti-gp120 (2G12-biotin), and mouse anti-p18 Gag IgG2a , together with the appropriate isotype controls.

Cytometry:

Article Title: The volatile anesthetic isoflurane perturbs conformational activation of integrin LFA-1 by binding to the allosteric regulatory cavity
Article Snippet: .. Bound ICAM-1 was detected by flow cytometry using a FACScan instrument (BD Bioscience, San Jose, CA USA). .. In some experiments, K562 cells expressing mutant LFA-1 (K287C/K294C) were pretreated with 20 mM dithiothreitol (DTT) for 10 min and then underwent continued treatment with 6.67 mM DTT during a 30-min incubation with soluble ICAM-1 .

Article Title: HIV gp120 induces endothelial dysfunction in tumour necrosis factor-?-activated porcine and human endothelial cells
Article Snippet: .. HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h. Cell surface expression levels of ICAM-1, CD40, CXCR-5, CCR5, and DC-SIGN were determined by FACScalibur flow cytometer (Becton Dickinson, Mountain View, CA, USA) equipped with CellQuest software (Becton Dickinson). ..

Blocking Assay:

Article Title: High-Multiplicity HIV-1 Infection and Neutralizing Antibody Evasion Mediated by the Macrophage-T Cell Virological Synapse
Article Snippet: .. For functional assays, blocking antibodies all were purified mouse IgG1 used at 10 μg/ml unless otherwise stated: CD4 (13B.8.2; Beckman-Coulter), CCR5 (2D7; BD Biosciences), ICAM-1 (LB-2 IgG2b ; BD Biosciences or Santa-Cruz), LFA-1 (L130; BD Biosciences), ICAM-2 (B-T1; AbD Serotec), and ICAM-3 (101-1D2; Santa-Cruz). .. For laser scanning confocal microscopy (LSCM), we used the following primary MAb: CD4 (nonblocking; clone L120; mouse IgG1; CFAR), CD81 (clone 454720; mouse IgG2b ; R & D Systems), anti-gp120 (2G12-biotin), and mouse anti-p18 Gag IgG2a , together with the appropriate isotype controls.

Purification:

Article Title: High-Multiplicity HIV-1 Infection and Neutralizing Antibody Evasion Mediated by the Macrophage-T Cell Virological Synapse
Article Snippet: .. For functional assays, blocking antibodies all were purified mouse IgG1 used at 10 μg/ml unless otherwise stated: CD4 (13B.8.2; Beckman-Coulter), CCR5 (2D7; BD Biosciences), ICAM-1 (LB-2 IgG2b ; BD Biosciences or Santa-Cruz), LFA-1 (L130; BD Biosciences), ICAM-2 (B-T1; AbD Serotec), and ICAM-3 (101-1D2; Santa-Cruz). .. For laser scanning confocal microscopy (LSCM), we used the following primary MAb: CD4 (nonblocking; clone L120; mouse IgG1; CFAR), CD81 (clone 454720; mouse IgG2b ; R & D Systems), anti-gp120 (2G12-biotin), and mouse anti-p18 Gag IgG2a , together with the appropriate isotype controls.

Activation Assay:

Article Title: Comparative Study of Brain CD8+ T Cells Induced by Sporozoites and Those Induced by Blood-Stage Plasmodium berghei ANKA Involved in the Development of Cerebral Malaria
Article Snippet: .. Biotinylated MAb directed against activation markers such as CD69 (H1.2F3), CD44 (IM7), CD62L (MEL-14), and adhesion molecules LFA-1 (M17/4) and ICAM-1 (3E2), allophycocyanin-conjugated anti-cytokine antibodies, anti-IFN-γ (XMG1.2), anti-TNF-α (MP6-XT22), anti-interleukin-4 (IL-4) (11B11) and anti-IL-10 (JES5-16E3) were purchased from BD-Pharmingen. .. Fluorescence-activated cell sorter (FACS) analysis was carried out using a FACScan cytofluorometer (Becton Dickinson, Grenoble, France), and data were processed with CellQuest software.

Incubation:

Article Title: Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression
Article Snippet: .. Followed by incubation with anti-ICAM-1 (mouse monoclonal antibody, cat. no. 554967; 1:50 dilution; BD Pharmingen; BD Biosciences, Franklin Lakes, NJ, USA), MMP-9 (mouse monoclonal antibody, cat. no. ab58803; 1:700 dilution; Abcam, Cambridge, UK), caspase-3 (rabbit polyclonal antibody, cat. no. 9662s; 1:700 dilution; Cell Signaling Technology, Inc., Danvers, MA, USA), and NF-κB-p65 (mouse monoclonal antibody, cat. no. 8242s; 1:800 dilution; Cell Signaling Technology, Inc.) antibodies at 4°C overnight. .. This was followed by incubations in a horseradish-peroxidase conjugated goat anti-mouse secondary antibody (cat. no. sc-2005; 1:2,000; Santa Cruz Biotechnology, Inc., Dallas, TX, USA) for 30 min at room temperature, or goat anti-rabbit secondary antibody (cat. no. sc-2054; 1:100; Santa Cruz Biotechnology, Inc.) for 1 h at room temperature.

Expressing:

Article Title: HIV gp120 induces endothelial dysfunction in tumour necrosis factor-?-activated porcine and human endothelial cells
Article Snippet: .. HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h. Cell surface expression levels of ICAM-1, CD40, CXCR-5, CCR5, and DC-SIGN were determined by FACScalibur flow cytometer (Becton Dickinson, Mountain View, CA, USA) equipped with CellQuest software (Becton Dickinson). ..

Staining:

Article Title: IL-11 Induces Encephalitogenic Th17 Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis
Article Snippet: .. The cells were harvested, fixed, permeabilized, and stained with fluorescently conjugated Abs against human IL-11 (R & D Systems), IL-17A, IFN-γ, (eBioscience), and CD4 (BD Bioscience) or murine IL-17A, IFN-γ, IL-4, TNF-α, IL-1β, IL-10, CD11b, CD8a, CD19 (eBioscience), Ly6C, CCR6, ICAM-1, VLA-4 and CD4 (BD Bioscience), GM-CSF (Miltenyi Biotec), IL-21, IL-21R, and IL-6R (R & D Systems). ..

Software:

Article Title: HIV gp120 induces endothelial dysfunction in tumour necrosis factor-?-activated porcine and human endothelial cells
Article Snippet: .. HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h. Cell surface expression levels of ICAM-1, CD40, CXCR-5, CCR5, and DC-SIGN were determined by FACScalibur flow cytometer (Becton Dickinson, Mountain View, CA, USA) equipped with CellQuest software (Becton Dickinson). ..

Immunofluorescence:

Article Title: Elevated levels of placental growth factor represent an adaptive host response in sepsis
Article Snippet: .. For double immunofluorescence, ICAM-1, COX-2, and PAI-1 antibodies were combined with rat monoclonal anti–mouse CD31 (BD Biosciences); VCAM-1, E-selectin, and P-selectin were combined with goat polyclonal anti–mouse CD31 antibody (Santa Cruz Biotechnology, Inc.. .. Secondary antibodies included anti–hamster IgG-FITC (Serotec), anti–rat IgG-Cy3 (Invitrogen), anti–rat IgG-FITC (Jackson ImmunoResearch Laboratories), anti–goat IgG-Cy3 (Jackson ImmunoResearch Laboratories), and anti–rabbit IgG-Cy3 (Invitrogen).

Flow Cytometry:

Article Title: The volatile anesthetic isoflurane perturbs conformational activation of integrin LFA-1 by binding to the allosteric regulatory cavity
Article Snippet: .. Bound ICAM-1 was detected by flow cytometry using a FACScan instrument (BD Bioscience, San Jose, CA USA). .. In some experiments, K562 cells expressing mutant LFA-1 (K287C/K294C) were pretreated with 20 mM dithiothreitol (DTT) for 10 min and then underwent continued treatment with 6.67 mM DTT during a 30-min incubation with soluble ICAM-1 .

Article Title: HIV gp120 induces endothelial dysfunction in tumour necrosis factor-?-activated porcine and human endothelial cells
Article Snippet: .. HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h. Cell surface expression levels of ICAM-1, CD40, CXCR-5, CCR5, and DC-SIGN were determined by FACScalibur flow cytometer (Becton Dickinson, Mountain View, CA, USA) equipped with CellQuest software (Becton Dickinson). ..

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    Becton Dickinson icam 1
    Expression of <t>ICAM-1</t> and HIV receptors/coreceptors and role of ICAM-1 silencing in HCAECs. ( A ) HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h, and the expression of ICAM-1 and HIV receptors or coreceptors including CD4, CXCR4, CCR5,
    Icam 1, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 92/100, based on 80 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Breast Cancer Cell Icam 1 Surface Protein Expression, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Disruption of actin filaments in target cells increases <t>ICAM-1</t> mobility. ICAM-1 mobility was determined by Fluorescence Recovery after Photobleaching (FRAP). Cells were stained with a PE-labeled anti-ICAM-1 antibody. Fluorescence recovery in the bleached
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    Expression of ICAM-1 and HIV receptors/coreceptors and role of ICAM-1 silencing in HCAECs. ( A ) HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h, and the expression of ICAM-1 and HIV receptors or coreceptors including CD4, CXCR4, CCR5,

    Journal: Cardiovascular Research

    Article Title: HIV gp120 induces endothelial dysfunction in tumour necrosis factor-?-activated porcine and human endothelial cells

    doi: 10.1093/cvr/cvq013

    Figure Lengend Snippet: Expression of ICAM-1 and HIV receptors/coreceptors and role of ICAM-1 silencing in HCAECs. ( A ) HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h, and the expression of ICAM-1 and HIV receptors or coreceptors including CD4, CXCR4, CCR5,

    Article Snippet: HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h. Cell surface expression levels of ICAM-1, CD40, CXCR-5, CCR5, and DC-SIGN were determined by FACScalibur flow cytometer (Becton Dickinson, Mountain View, CA, USA) equipped with CellQuest software (Becton Dickinson).

    Techniques: Expressing

    Effects of HIV gp120, TNF-α, anti-gp120, and anti-ICAM-1 antibodies on eNOS expression in HCAECs. Cells were pretreated with TNF-α for 8 h and followed by HIV gp120, HIV gp120 plus anti-gp120 antibody or HIV gp120 plus anti-ICAM-1 antibody

    Journal: Cardiovascular Research

    Article Title: HIV gp120 induces endothelial dysfunction in tumour necrosis factor-?-activated porcine and human endothelial cells

    doi: 10.1093/cvr/cvq013

    Figure Lengend Snippet: Effects of HIV gp120, TNF-α, anti-gp120, and anti-ICAM-1 antibodies on eNOS expression in HCAECs. Cells were pretreated with TNF-α for 8 h and followed by HIV gp120, HIV gp120 plus anti-gp120 antibody or HIV gp120 plus anti-ICAM-1 antibody

    Article Snippet: HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h. Cell surface expression levels of ICAM-1, CD40, CXCR-5, CCR5, and DC-SIGN were determined by FACScalibur flow cytometer (Becton Dickinson, Mountain View, CA, USA) equipped with CellQuest software (Becton Dickinson).

    Techniques: Expressing

    Blocking effects of anti-gp120 and anti-ICAM-1 antibodies on HIV gp120-induced decrease in vasomotor function and eNOS expression in TNF-α-pretreated porcine coronary arteries. Porcine coronary artery rings were treated with TNF-α for

    Journal: Cardiovascular Research

    Article Title: HIV gp120 induces endothelial dysfunction in tumour necrosis factor-?-activated porcine and human endothelial cells

    doi: 10.1093/cvr/cvq013

    Figure Lengend Snippet: Blocking effects of anti-gp120 and anti-ICAM-1 antibodies on HIV gp120-induced decrease in vasomotor function and eNOS expression in TNF-α-pretreated porcine coronary arteries. Porcine coronary artery rings were treated with TNF-α for

    Article Snippet: HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h. Cell surface expression levels of ICAM-1, CD40, CXCR-5, CCR5, and DC-SIGN were determined by FACScalibur flow cytometer (Becton Dickinson, Mountain View, CA, USA) equipped with CellQuest software (Becton Dickinson).

    Techniques: Blocking Assay, Expressing

    Effects of HIV gp120 and TNF-α on the immunoreactivity of eNOS and ICAM-1 in porcine coronary arteries. Porcine coronary artery rings were treated with TNF-α for 8 h and/or HIV gp120 for 16 h. Porcine coronary artery rings were fixed in

    Journal: Cardiovascular Research

    Article Title: HIV gp120 induces endothelial dysfunction in tumour necrosis factor-?-activated porcine and human endothelial cells

    doi: 10.1093/cvr/cvq013

    Figure Lengend Snippet: Effects of HIV gp120 and TNF-α on the immunoreactivity of eNOS and ICAM-1 in porcine coronary arteries. Porcine coronary artery rings were treated with TNF-α for 8 h and/or HIV gp120 for 16 h. Porcine coronary artery rings were fixed in

    Article Snippet: HCAECs were treated with or without TNF-α (2 ng/mL) for 8 h. Cell surface expression levels of ICAM-1, CD40, CXCR-5, CCR5, and DC-SIGN were determined by FACScalibur flow cytometer (Becton Dickinson, Mountain View, CA, USA) equipped with CellQuest software (Becton Dickinson).

    Techniques:

    Identification of ICAM-1 as a TNBC target and biomarker. ( A ) Gene expression analysis of human breast cancer cell lines. Red and green represent maximum and minimum gene expression, respectively. Representative microscopic images of human TNBC tissues

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: ICAM-1 as a molecular target for triple negative breast cancer

    doi: 10.1073/pnas.1408556111

    Figure Lengend Snippet: Identification of ICAM-1 as a TNBC target and biomarker. ( A ) Gene expression analysis of human breast cancer cell lines. Red and green represent maximum and minimum gene expression, respectively. Representative microscopic images of human TNBC tissues

    Article Snippet: Breast cancer cell ICAM-1 surface protein expression was evaluated by a BD FACSCalibur flow cytometer (BD Biosciences) as described previously ( , ).

    Techniques: Biomarker Assay, Expressing

    In vivo MR detection of TNBC using ICAM-1 targeting MRI probes. ( A ) Color maps of T 2 -weighted MR images of a mouse implanted with the TNBC cell line MDA-MB-231 at different time points (pre, 24 h, and 48 h) after injection of IGG-IONP, or HER2-IONP, or

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: ICAM-1 as a molecular target for triple negative breast cancer

    doi: 10.1073/pnas.1408556111

    Figure Lengend Snippet: In vivo MR detection of TNBC using ICAM-1 targeting MRI probes. ( A ) Color maps of T 2 -weighted MR images of a mouse implanted with the TNBC cell line MDA-MB-231 at different time points (pre, 24 h, and 48 h) after injection of IGG-IONP, or HER2-IONP, or

    Article Snippet: Breast cancer cell ICAM-1 surface protein expression was evaluated by a BD FACSCalibur flow cytometer (BD Biosciences) as described previously ( , ).

    Techniques: In Vivo, Magnetic Resonance Imaging, Multiple Displacement Amplification, Injection

    Blockade of A-SAA–induced ICAM-1 on RA FLCs by specific anti–SR-B1 antibody. Four separate primary RA FLC lines stimulated for 24 hours in duplicate with A-SAA (10 μg/ml) in the presence or absence of anti-SR-B1antibody (10 μg/ml).

    Journal: The American Journal of Pathology

    Article Title: A Role for the High-Density Lipoprotein Receptor SR-B1 in Synovial Inflammation via Serum Amyloid-A

    doi: 10.2353/ajpath.2010.090014

    Figure Lengend Snippet: Blockade of A-SAA–induced ICAM-1 on RA FLCs by specific anti–SR-B1 antibody. Four separate primary RA FLC lines stimulated for 24 hours in duplicate with A-SAA (10 μg/ml) in the presence or absence of anti-SR-B1antibody (10 μg/ml).

    Article Snippet: Cells were transferred to fluorescence-activated cell sorting tubes (Becton Dickinson, Franklin Lakes, NJ) and incubated with 0.3 μg/ml of phycoerythrin-conjugated monoclonal mouse anti–ICAM-1 (Becton Dickenson), anti–VCAM-1 (Becton Dickenson), or an appropriate isotype-IgG matched control (Becton Dickinson) for 30 minutes at 4°C.

    Techniques:

    Synthetic mimetic peptides of ApoA-1 block A-SAA–induced VCAM-1 and ICAM-1 on HMVECs. HMVECs were incubated with A-SAA in the presence of increasing peptide concentrations. A – D: ApoA-1 mimetic peptides L-37pA(5 μg/ml) and D-37pA

    Journal: The American Journal of Pathology

    Article Title: A Role for the High-Density Lipoprotein Receptor SR-B1 in Synovial Inflammation via Serum Amyloid-A

    doi: 10.2353/ajpath.2010.090014

    Figure Lengend Snippet: Synthetic mimetic peptides of ApoA-1 block A-SAA–induced VCAM-1 and ICAM-1 on HMVECs. HMVECs were incubated with A-SAA in the presence of increasing peptide concentrations. A – D: ApoA-1 mimetic peptides L-37pA(5 μg/ml) and D-37pA

    Article Snippet: Cells were transferred to fluorescence-activated cell sorting tubes (Becton Dickinson, Franklin Lakes, NJ) and incubated with 0.3 μg/ml of phycoerythrin-conjugated monoclonal mouse anti–ICAM-1 (Becton Dickenson), anti–VCAM-1 (Becton Dickenson), or an appropriate isotype-IgG matched control (Becton Dickinson) for 30 minutes at 4°C.

    Techniques: Blocking Assay, Incubation

    Blockade of A-SAA–induced ICAM-1 on HMVECs by specific anti–SR-B1 antibody. HMVECs ( n = 3) were stimulated with A-SAA for 24 hours (1 to 10 μg/ml) in the presence or absence of anti–SR-B1 (10 μg/ml) antibody

    Journal: The American Journal of Pathology

    Article Title: A Role for the High-Density Lipoprotein Receptor SR-B1 in Synovial Inflammation via Serum Amyloid-A

    doi: 10.2353/ajpath.2010.090014

    Figure Lengend Snippet: Blockade of A-SAA–induced ICAM-1 on HMVECs by specific anti–SR-B1 antibody. HMVECs ( n = 3) were stimulated with A-SAA for 24 hours (1 to 10 μg/ml) in the presence or absence of anti–SR-B1 (10 μg/ml) antibody

    Article Snippet: Cells were transferred to fluorescence-activated cell sorting tubes (Becton Dickinson, Franklin Lakes, NJ) and incubated with 0.3 μg/ml of phycoerythrin-conjugated monoclonal mouse anti–ICAM-1 (Becton Dickenson), anti–VCAM-1 (Becton Dickenson), or an appropriate isotype-IgG matched control (Becton Dickinson) for 30 minutes at 4°C.

    Techniques:

    Disruption of actin filaments in target cells increases ICAM-1 mobility. ICAM-1 mobility was determined by Fluorescence Recovery after Photobleaching (FRAP). Cells were stained with a PE-labeled anti-ICAM-1 antibody. Fluorescence recovery in the bleached

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

    Article Title: Tethering of ICAM on target cells is required for LFA-1-dependent NK cell adhesion and granule polarization

    doi: 10.4049/jimmunol.1000761

    Figure Lengend Snippet: Disruption of actin filaments in target cells increases ICAM-1 mobility. ICAM-1 mobility was determined by Fluorescence Recovery after Photobleaching (FRAP). Cells were stained with a PE-labeled anti-ICAM-1 antibody. Fluorescence recovery in the bleached

    Article Snippet: ICAM-1 on 721.221 cells was stained using a PE-conjugated anti-ICAM-1 antibody (Becton Dickinson).

    Techniques: Fluorescence, Staining, Labeling

    Movement of human resting NK cells over mobile and immobile ICAM-1. NK cells were visualized 20 minutes after injection into chambers containing ICAM-1 bound to either lipid bilayers or glass surfaces, respectively. The movement of NK cells was tracked

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

    Article Title: Tethering of ICAM on target cells is required for LFA-1-dependent NK cell adhesion and granule polarization

    doi: 10.4049/jimmunol.1000761

    Figure Lengend Snippet: Movement of human resting NK cells over mobile and immobile ICAM-1. NK cells were visualized 20 minutes after injection into chambers containing ICAM-1 bound to either lipid bilayers or glass surfaces, respectively. The movement of NK cells was tracked

    Article Snippet: ICAM-1 on 721.221 cells was stained using a PE-conjugated anti-ICAM-1 antibody (Becton Dickinson).

    Techniques: Injection

    Disruption of actin filaments increases the mobility of ICAM-1 and ICAM-2. The mobility of ICAM-1 ( A , upper panel, bar indicates 5 μm, B and D , left side) and ICAM-2 ( A , lower panel, B and D , right side) in 721.221 cells treated with the indicated

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

    Article Title: Tethering of ICAM on target cells is required for LFA-1-dependent NK cell adhesion and granule polarization

    doi: 10.4049/jimmunol.1000761

    Figure Lengend Snippet: Disruption of actin filaments increases the mobility of ICAM-1 and ICAM-2. The mobility of ICAM-1 ( A , upper panel, bar indicates 5 μm, B and D , left side) and ICAM-2 ( A , lower panel, B and D , right side) in 721.221 cells treated with the indicated

    Article Snippet: ICAM-1 on 721.221 cells was stained using a PE-conjugated anti-ICAM-1 antibody (Becton Dickinson).

    Techniques:

    Disruption of actin filaments increases the mobility of ICAM-1 on K562 cells and decreases conjugate formation with NK cells. The mobility of ICAM-1 was determined by FRAP. Cells were stained with a PE-labeled anti-ICAM-1 antibody. Fluorescence recovery

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

    Article Title: Tethering of ICAM on target cells is required for LFA-1-dependent NK cell adhesion and granule polarization

    doi: 10.4049/jimmunol.1000761

    Figure Lengend Snippet: Disruption of actin filaments increases the mobility of ICAM-1 on K562 cells and decreases conjugate formation with NK cells. The mobility of ICAM-1 was determined by FRAP. Cells were stained with a PE-labeled anti-ICAM-1 antibody. Fluorescence recovery

    Article Snippet: ICAM-1 on 721.221 cells was stained using a PE-conjugated anti-ICAM-1 antibody (Becton Dickinson).

    Techniques: Staining, Labeling, Fluorescence