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Effect of DYSGT on ET-1, <t>ICAM-1,</t> and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P
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1) Product Images from "Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis"

Article Title: Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis

Journal: Evidence-based Complementary and Alternative Medicine : eCAM

doi: 10.1155/2013/783576

Effect of DYSGT on ET-1, ICAM-1, and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P
Figure Legend Snippet: Effect of DYSGT on ET-1, ICAM-1, and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P

Techniques Used: Expressing, Mouse Assay, Western Blot

Immunofluorescence staining of (a) ICAM-1 and (b) ET-1 in the aorta. Representative histological sections are thoracic aorta of Cont., ApoE KO mice, ApoE mice treated with rosiglitazone, and ApoE mice treated with DYSGT incubated with anti-ICAM-1, anti-ET-1 antibodies, respectively. Original magnification: 100x.
Figure Legend Snippet: Immunofluorescence staining of (a) ICAM-1 and (b) ET-1 in the aorta. Representative histological sections are thoracic aorta of Cont., ApoE KO mice, ApoE mice treated with rosiglitazone, and ApoE mice treated with DYSGT incubated with anti-ICAM-1, anti-ET-1 antibodies, respectively. Original magnification: 100x.

Techniques Used: Immunofluorescence, Staining, Mouse Assay, Incubation

2) Product Images from "Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis"

Article Title: Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis

Journal: Evidence-based Complementary and Alternative Medicine : eCAM

doi: 10.1155/2013/783576

Effect of DYSGT on ET-1, ICAM-1, and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P
Figure Legend Snippet: Effect of DYSGT on ET-1, ICAM-1, and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P

Techniques Used: Expressing, Mouse Assay, Western Blot

Immunofluorescence staining of (a) ICAM-1 and (b) ET-1 in the aorta. Representative histological sections are thoracic aorta of Cont., ApoE KO mice, ApoE mice treated with rosiglitazone, and ApoE mice treated with DYSGT incubated with anti-ICAM-1, anti-ET-1 antibodies, respectively. Original magnification: 100x.
Figure Legend Snippet: Immunofluorescence staining of (a) ICAM-1 and (b) ET-1 in the aorta. Representative histological sections are thoracic aorta of Cont., ApoE KO mice, ApoE mice treated with rosiglitazone, and ApoE mice treated with DYSGT incubated with anti-ICAM-1, anti-ET-1 antibodies, respectively. Original magnification: 100x.

Techniques Used: Immunofluorescence, Staining, Mouse Assay, Incubation

3) Product Images from "Reduced immune cell infiltration and increased pro-inflammatory mediators in the brain of Type 2 diabetic mouse model infected with West Nile virus"

Article Title: Reduced immune cell infiltration and increased pro-inflammatory mediators in the brain of Type 2 diabetic mouse model infected with West Nile virus

Journal: Journal of Neuroinflammation

doi: 10.1186/1742-2094-11-80

WNV-induced CAM expression in the brains of WT and db / db mice. (A) qRT-PCR was conducted on RNA extracted from mock- and WNV-infected brains from WT and db/db mice at indicated time points to determine the fold-change in E-selectin , ICAM-1 , and VCAM-1 gene expression. Changes in the levels of each gene were first normalized to the β-actin gene, and then the fold-change in WNV-infected brains was calculated in comparison to corresponding mock-infected brains. Data represents the mean ± SEM, representing two independent experiments (n = 7 per group). * P
Figure Legend Snippet: WNV-induced CAM expression in the brains of WT and db / db mice. (A) qRT-PCR was conducted on RNA extracted from mock- and WNV-infected brains from WT and db/db mice at indicated time points to determine the fold-change in E-selectin , ICAM-1 , and VCAM-1 gene expression. Changes in the levels of each gene were first normalized to the β-actin gene, and then the fold-change in WNV-infected brains was calculated in comparison to corresponding mock-infected brains. Data represents the mean ± SEM, representing two independent experiments (n = 7 per group). * P

Techniques Used: Chick Chorioallantoic Membrane Assay, Expressing, Mouse Assay, Quantitative RT-PCR, Infection

Immunohistochemical analysis of CAM in the brains of WT and db / db mice after WNV infection. Cryopreserved brain sections from WNV-infected WT and db/db mice at day 8 after infection were stained with antibodies against E-selectin, ICAM-1, VCAM-1 (Red), and vWF (Green). The photomicrographs demonstrate representative images obtained from two independent experiments (n = 4 per group). Bars, 20 μm. ICAM-1, intercellular cell adhesion molecule 1; VCAM-1, vascular cell adhesion molecule 1; vWF, von Willebrand factor.
Figure Legend Snippet: Immunohistochemical analysis of CAM in the brains of WT and db / db mice after WNV infection. Cryopreserved brain sections from WNV-infected WT and db/db mice at day 8 after infection were stained with antibodies against E-selectin, ICAM-1, VCAM-1 (Red), and vWF (Green). The photomicrographs demonstrate representative images obtained from two independent experiments (n = 4 per group). Bars, 20 μm. ICAM-1, intercellular cell adhesion molecule 1; VCAM-1, vascular cell adhesion molecule 1; vWF, von Willebrand factor.

Techniques Used: Immunohistochemistry, Chick Chorioallantoic Membrane Assay, Mouse Assay, Infection, Staining

4) Product Images from "Reduced immune cell infiltration and increased pro-inflammatory mediators in the brain of Type 2 diabetic mouse model infected with West Nile virus"

Article Title: Reduced immune cell infiltration and increased pro-inflammatory mediators in the brain of Type 2 diabetic mouse model infected with West Nile virus

Journal: Journal of Neuroinflammation

doi: 10.1186/1742-2094-11-80

WNV-induced CAM expression in the brains of WT and db / db mice. (A) qRT-PCR was conducted on RNA extracted from mock- and WNV-infected brains from WT and db/db mice at indicated time points to determine the fold-change in E-selectin , ICAM-1 , and VCAM-1 gene expression. Changes in the levels of each gene were first normalized to the β-actin gene, and then the fold-change in WNV-infected brains was calculated in comparison to corresponding mock-infected brains. Data represents the mean ± SEM, representing two independent experiments (n = 7 per group). * P
Figure Legend Snippet: WNV-induced CAM expression in the brains of WT and db / db mice. (A) qRT-PCR was conducted on RNA extracted from mock- and WNV-infected brains from WT and db/db mice at indicated time points to determine the fold-change in E-selectin , ICAM-1 , and VCAM-1 gene expression. Changes in the levels of each gene were first normalized to the β-actin gene, and then the fold-change in WNV-infected brains was calculated in comparison to corresponding mock-infected brains. Data represents the mean ± SEM, representing two independent experiments (n = 7 per group). * P

Techniques Used: Chick Chorioallantoic Membrane Assay, Expressing, Mouse Assay, Quantitative RT-PCR, Infection

Immunohistochemical analysis of CAM in the brains of WT and db / db mice after WNV infection. Cryopreserved brain sections from WNV-infected WT and db/db mice at day 8 after infection were stained with antibodies against E-selectin, ICAM-1, VCAM-1 (Red), and vWF (Green). The photomicrographs demonstrate representative images obtained from two independent experiments (n = 4 per group). Bars, 20 μm. ICAM-1, intercellular cell adhesion molecule 1; VCAM-1, vascular cell adhesion molecule 1; vWF, von Willebrand factor.
Figure Legend Snippet: Immunohistochemical analysis of CAM in the brains of WT and db / db mice after WNV infection. Cryopreserved brain sections from WNV-infected WT and db/db mice at day 8 after infection were stained with antibodies against E-selectin, ICAM-1, VCAM-1 (Red), and vWF (Green). The photomicrographs demonstrate representative images obtained from two independent experiments (n = 4 per group). Bars, 20 μm. ICAM-1, intercellular cell adhesion molecule 1; VCAM-1, vascular cell adhesion molecule 1; vWF, von Willebrand factor.

Techniques Used: Immunohistochemistry, Chick Chorioallantoic Membrane Assay, Mouse Assay, Infection, Staining

5) Product Images from "The 18-kDa Translocator Protein Inhibits Vascular Cell Adhesion Molecule-1 Expression via Inhibition of Mitochondrial Reactive Oxygen Species"

Article Title: The 18-kDa Translocator Protein Inhibits Vascular Cell Adhesion Molecule-1 Expression via Inhibition of Mitochondrial Reactive Oxygen Species

Journal: Molecules and Cells

doi: 10.14348/molcells.2015.0165

TSPO overexpression inhibited PMA-induced VCAM-1 and ICAM-1 expression in endothelial cells. (A) HUVECs transfected with AdTSPO were treated with 250 nM PMA for 6 h, followed by Western blot analysis of the cell lysates. The total adenoviral MOI of 100 was balanced in the Adβgal control. FLAG-tagged TSPO over-expression was confirmed by anti-TSPO antibody detection. The β–actin was used as a loading control. (B) Densitometric analysis of Western blots. Data are expressed as percent densitometric values of VCAM-1 expression induced by PMA. Each bar represents mean ± SEM (n = 4). * p
Figure Legend Snippet: TSPO overexpression inhibited PMA-induced VCAM-1 and ICAM-1 expression in endothelial cells. (A) HUVECs transfected with AdTSPO were treated with 250 nM PMA for 6 h, followed by Western blot analysis of the cell lysates. The total adenoviral MOI of 100 was balanced in the Adβgal control. FLAG-tagged TSPO over-expression was confirmed by anti-TSPO antibody detection. The β–actin was used as a loading control. (B) Densitometric analysis of Western blots. Data are expressed as percent densitometric values of VCAM-1 expression induced by PMA. Each bar represents mean ± SEM (n = 4). * p

Techniques Used: Over Expression, Expressing, Transfection, Western Blot

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

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

Journal: BMC Microbiology

doi: 10.1186/s12866-014-0229-z

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

Techniques Used: Transfection, Expressing, Incubation, Staining

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

Techniques Used: Incubation, Staining, Expressing, Western Blot

7) Product Images from "Expression of Intercellular Adhesion Molecule-1 and E-Selectin in Gastric Cancer and Their Clinical Significance"

Article Title: Expression of Intercellular Adhesion Molecule-1 and E-Selectin in Gastric Cancer and Their Clinical Significance

Journal: Journal of Gastric Cancer

doi: 10.5230/jgc.2012.12.3.140

(A) Overall 3-year survival of gastric cancer patients according to the intercellular adhesion molecule-1 (ICAM-1) immune reactivity. (B) Disease-free 3-year survival of gastric cancer patients according to the ICAM-1 immune reactivity.
Figure Legend Snippet: (A) Overall 3-year survival of gastric cancer patients according to the intercellular adhesion molecule-1 (ICAM-1) immune reactivity. (B) Disease-free 3-year survival of gastric cancer patients according to the ICAM-1 immune reactivity.

Techniques Used:

Immunohistochemical staining of intercellular adhesion molecule-1 (ICAM-1), E-selectin in tissue microarray slides of gastric cancer. (A) Expression of ICAM-1 was noted in the endothelial cells of gastric cancer tissues. More than 50% of cancer cells were stained (×400). (B) Expression of E-selectin was noted in the diffuse type signet ring gastric cancer cells. More than 50% were stained (×400).
Figure Legend Snippet: Immunohistochemical staining of intercellular adhesion molecule-1 (ICAM-1), E-selectin in tissue microarray slides of gastric cancer. (A) Expression of ICAM-1 was noted in the endothelial cells of gastric cancer tissues. More than 50% of cancer cells were stained (×400). (B) Expression of E-selectin was noted in the diffuse type signet ring gastric cancer cells. More than 50% were stained (×400).

Techniques Used: Immunohistochemistry, Staining, Microarray, Expressing

Intercellular adhesion molecule-1 (ICAM-1), E-selectin expression level in gastric cancer tissues and cell lines (MKN28, KATO3). (A) CAM-1 expression was noted in normal stomach tissues but it was increased in gastric cancer tissues and cultured gastric cancer cells. (B) E-selectin expression was more prominent in normal stomach tissues but it was decreased in gastric cancer tissues and cultured gastric cancer cells.
Figure Legend Snippet: Intercellular adhesion molecule-1 (ICAM-1), E-selectin expression level in gastric cancer tissues and cell lines (MKN28, KATO3). (A) CAM-1 expression was noted in normal stomach tissues but it was increased in gastric cancer tissues and cultured gastric cancer cells. (B) E-selectin expression was more prominent in normal stomach tissues but it was decreased in gastric cancer tissues and cultured gastric cancer cells.

Techniques Used: Expressing, Chick Chorioallantoic Membrane Assay, Cell Culture

8) Product Images from "The involvement of high mobility group 1 cytokine and phospholipases A2 in diabetic retinopathy"

Article Title: The involvement of high mobility group 1 cytokine and phospholipases A2 in diabetic retinopathy

Journal: Lipids in Health and Disease

doi: 10.1186/1476-511X-13-156

Represent the western blot detecting the protein levels of A. HMGB1, B. PLA2, C. IL-1β, D. TNF-α, E. VEGF, and F. ICAM-1 with the quantification of their corresponding band intensity from the retinal tissue of control and diabetic retinopathy rats.
Figure Legend Snippet: Represent the western blot detecting the protein levels of A. HMGB1, B. PLA2, C. IL-1β, D. TNF-α, E. VEGF, and F. ICAM-1 with the quantification of their corresponding band intensity from the retinal tissue of control and diabetic retinopathy rats.

Techniques Used: Western Blot

Represent the mRNA expression of HMGB1, PLA2, TNF-α, VEGF, ICAM-1 from the retinal tissue of control and diabetic retinopathy rats.
Figure Legend Snippet: Represent the mRNA expression of HMGB1, PLA2, TNF-α, VEGF, ICAM-1 from the retinal tissue of control and diabetic retinopathy rats.

Techniques Used: Expressing

9) Product Images from "The involvement of high mobility group 1 cytokine and phospholipases A2 in diabetic retinopathy"

Article Title: The involvement of high mobility group 1 cytokine and phospholipases A2 in diabetic retinopathy

Journal: Lipids in Health and Disease

doi: 10.1186/1476-511X-13-156

Represent the western blot detecting the protein levels of A. HMGB1, B. PLA2, C. IL-1β, D. TNF-α, E. VEGF, and F. ICAM-1 with the quantification of their corresponding band intensity from the retinal tissue of control and diabetic retinopathy rats.
Figure Legend Snippet: Represent the western blot detecting the protein levels of A. HMGB1, B. PLA2, C. IL-1β, D. TNF-α, E. VEGF, and F. ICAM-1 with the quantification of their corresponding band intensity from the retinal tissue of control and diabetic retinopathy rats.

Techniques Used: Western Blot

Represent the mRNA expression of HMGB1, PLA2, TNF-α, VEGF, ICAM-1 from the retinal tissue of control and diabetic retinopathy rats.
Figure Legend Snippet: Represent the mRNA expression of HMGB1, PLA2, TNF-α, VEGF, ICAM-1 from the retinal tissue of control and diabetic retinopathy rats.

Techniques Used: Expressing

10) Product Images from "Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow"

Article Title: Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow

Journal: PLoS ONE

doi: 10.1371/journal.pone.0167576

Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.
Figure Legend Snippet: Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.

Techniques Used: Flow Cytometry, Activity Assay, Activation Assay

ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p
Figure Legend Snippet: ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p

Techniques Used: Expressing, Flow Cytometry, Western Blot

11) Product Images from "Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow"

Article Title: Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow

Journal: PLoS ONE

doi: 10.1371/journal.pone.0167576

Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.
Figure Legend Snippet: Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.

Techniques Used: Flow Cytometry, Activity Assay, Activation Assay

ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p
Figure Legend Snippet: ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p

Techniques Used: Expressing, Flow Cytometry, Western Blot

12) Product Images from "Helicobacter pylori Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a β2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism"

Article Title: Helicobacter pylori Outer Membrane Vesicle Proteins Induce Human Eosinophil Degranulation via a β2 Integrin CD11/CD18- and ICAM-1-Dependent Mechanism

Journal: Mediators of Inflammation

doi: 10.1155/2015/301716

ICAM-1 expression in gastric epithelial cells stimulated with H. pylori OMVs or OMV-induced culture supernatant. (a) OMV-CM and control-CM were prepared as described in Materials and Methods. Primary human gastric epithelial cells were stimulated with OMVs (200 μ g/mL), OMV-CM (50% v/v), or control CM (50% v/v) for 24 h. Cells were stained with a mAb against ICAM-1 and then analyzed using flow cytometry. Results are representative of more than five independent experiments. (b) Time course of ICAM-1 mRNA expression in gastric epithelial cells after stimulation with OMVs, OMV-CM, or control-CM. Cells were stimulated with OMVs (200 μ g/mL), OMV-CM (50% v/v), or control-CM (50% v/v) for the indicated periods of time. The expression levels of ICAM-1 and β -actin mRNA were analyzed by quantitative RT-PCR using standard RNAs. Values are expressed as mean ± SD ( n = 5). Asterisks indicate statistical significance after comparison with unstimulated controls ( P
Figure Legend Snippet: ICAM-1 expression in gastric epithelial cells stimulated with H. pylori OMVs or OMV-induced culture supernatant. (a) OMV-CM and control-CM were prepared as described in Materials and Methods. Primary human gastric epithelial cells were stimulated with OMVs (200 μ g/mL), OMV-CM (50% v/v), or control CM (50% v/v) for 24 h. Cells were stained with a mAb against ICAM-1 and then analyzed using flow cytometry. Results are representative of more than five independent experiments. (b) Time course of ICAM-1 mRNA expression in gastric epithelial cells after stimulation with OMVs, OMV-CM, or control-CM. Cells were stimulated with OMVs (200 μ g/mL), OMV-CM (50% v/v), or control-CM (50% v/v) for the indicated periods of time. The expression levels of ICAM-1 and β -actin mRNA were analyzed by quantitative RT-PCR using standard RNAs. Values are expressed as mean ± SD ( n = 5). Asterisks indicate statistical significance after comparison with unstimulated controls ( P

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

Relationship between ICAM-1 suppression and ECP release from eosinophils. (a) Primary human gastric epithelial cells were transduced with lentivirus harboring either shRNA directed against ICAM-1 or control shRNA. Transduced cells were then stimulated with TNF- α (20 ng/mL) for 1 h. The cellular levels of ICAM-1 and actin were determined by immunoblot analysis. Results are representative of more than three independent experiments. (b) Transduced or nontransduced gastric epithelial cells were stimulated with OMVs (200 μ g/mL), OMV-CM (50% v/v), or control-CM (50% v/v) for 24 h. Cells were stained with a mAb against ICAM-1 and then analyzed by flow cytometry. Data are represented as MFI ± SEM ( n = 5). (c) Transduced or nontransduced gastric epithelial cells were exposed to OMVs (200 μ g/mL) for 24 h and then washed twice in PBS. OMV-exposed gastric epithelial cells were cocultured with human eosinophils for 24 h (left panel). Transduced or nontransduced gastric epithelial cells were stimulated with control-CM (50% v/v) or OMV-CM (50% v/v) for 24 h and then washed twice in PBS. Finally, human eosinophils were cocultured with either control-CM-stimulated or OMV-CM-stimulated epithelial cells for 24 h (right panel). The concentration of ECP in each culture supernatant was measured by ELISA (mean ± SEM, n = 5). * P
Figure Legend Snippet: Relationship between ICAM-1 suppression and ECP release from eosinophils. (a) Primary human gastric epithelial cells were transduced with lentivirus harboring either shRNA directed against ICAM-1 or control shRNA. Transduced cells were then stimulated with TNF- α (20 ng/mL) for 1 h. The cellular levels of ICAM-1 and actin were determined by immunoblot analysis. Results are representative of more than three independent experiments. (b) Transduced or nontransduced gastric epithelial cells were stimulated with OMVs (200 μ g/mL), OMV-CM (50% v/v), or control-CM (50% v/v) for 24 h. Cells were stained with a mAb against ICAM-1 and then analyzed by flow cytometry. Data are represented as MFI ± SEM ( n = 5). (c) Transduced or nontransduced gastric epithelial cells were exposed to OMVs (200 μ g/mL) for 24 h and then washed twice in PBS. OMV-exposed gastric epithelial cells were cocultured with human eosinophils for 24 h (left panel). Transduced or nontransduced gastric epithelial cells were stimulated with control-CM (50% v/v) or OMV-CM (50% v/v) for 24 h and then washed twice in PBS. Finally, human eosinophils were cocultured with either control-CM-stimulated or OMV-CM-stimulated epithelial cells for 24 h (right panel). The concentration of ECP in each culture supernatant was measured by ELISA (mean ± SEM, n = 5). * P

Techniques Used: Transduction, shRNA, Staining, Flow Cytometry, Cytometry, Concentration Assay, Enzyme-linked Immunosorbent Assay

13) Product Images from "7-Ketocholesterol enhances leukocyte adhesion to endothelial cells via p38MAPK pathway"

Article Title: 7-Ketocholesterol enhances leukocyte adhesion to endothelial cells via p38MAPK pathway

Journal: PLoS ONE

doi: 10.1371/journal.pone.0200499

7-Ketocholesterol increases the expression of adhesion molecules and cytokines in human umbilical vascular endothelial cells (HUVECs). (A) HUVECs were pretreated with 50 μM 7-ketocholesterol or cholesterol or ethanol alone for 18 h, followed by stimulation with or without 0.1 ng/ml tumor necrosis factor (TNF)-α for an additional 4 h. The levels of E-selectin, ICAM-1, and VCAM-1 protein expression were analyzed by western blotting. Representative blots from three independent experiments are shown. (B) HUVECs were pretreated with 50 μM 7-ketocholesterol or cholesterol or ethanol alone for 18 h, followed by stimulation with or without 0.1 ng/ml TNF-α for an additional 2 h. IL-8 and MCP-1 mRNA levels were analyzed by RT-qPCR. Data are shown as mean ± standard errors of the means. *p
Figure Legend Snippet: 7-Ketocholesterol increases the expression of adhesion molecules and cytokines in human umbilical vascular endothelial cells (HUVECs). (A) HUVECs were pretreated with 50 μM 7-ketocholesterol or cholesterol or ethanol alone for 18 h, followed by stimulation with or without 0.1 ng/ml tumor necrosis factor (TNF)-α for an additional 4 h. The levels of E-selectin, ICAM-1, and VCAM-1 protein expression were analyzed by western blotting. Representative blots from three independent experiments are shown. (B) HUVECs were pretreated with 50 μM 7-ketocholesterol or cholesterol or ethanol alone for 18 h, followed by stimulation with or without 0.1 ng/ml TNF-α for an additional 2 h. IL-8 and MCP-1 mRNA levels were analyzed by RT-qPCR. Data are shown as mean ± standard errors of the means. *p

Techniques Used: Expressing, Western Blot, Quantitative RT-PCR

14) Product Images from "Progestin and AdipoQ Receptor 3 Upregulates Fibronectin and Intercellular Adhesion Molecule-1 in Glomerular Mesangial Cells via Activating NF-κB Signaling Pathway Under High Glucose Conditions"

Article Title: Progestin and AdipoQ Receptor 3 Upregulates Fibronectin and Intercellular Adhesion Molecule-1 in Glomerular Mesangial Cells via Activating NF-κB Signaling Pathway Under High Glucose Conditions

Journal: Frontiers in Endocrinology

doi: 10.3389/fendo.2018.00275

Genetical and pharmacological inhibition of NF-κB attenuated the effects of progestin and adipoQ receptor 3 (PAQR3) overexpression on high glucose (HG)-induced upregulation of fibronectin and intercellular adhesion molecule-1. Glomerular mesangial cells (GMCs) were transfected with si-NF-κB and PAQR3 plasmid for 24 h, then treated with HG for 24 h and total proteins were harvested to Western blot assay  (A,B) .  ### P
Figure Legend Snippet: Genetical and pharmacological inhibition of NF-κB attenuated the effects of progestin and adipoQ receptor 3 (PAQR3) overexpression on high glucose (HG)-induced upregulation of fibronectin and intercellular adhesion molecule-1. Glomerular mesangial cells (GMCs) were transfected with si-NF-κB and PAQR3 plasmid for 24 h, then treated with HG for 24 h and total proteins were harvested to Western blot assay (A,B) . ### P

Techniques Used: Inhibition, Over Expression, Transfection, Plasmid Preparation, Western Blot

Overexpression of progestin and adipoQ receptor 3 (PAQR3) induced the expressions of fibronectin (FN), intercellular adhesion molecule-1 (ICAM-1) in high glucose (HG)-cultured glomerular mesangial cells (GMCs). GMCs were transfected with 2 µg of Penter vector or his-PAQR3, respectively. After treatment with HG for 24 h, total proteins were extracted to measure expressions of PAQR3, FN, and ICAM-1 (A,B) . ### P
Figure Legend Snippet: Overexpression of progestin and adipoQ receptor 3 (PAQR3) induced the expressions of fibronectin (FN), intercellular adhesion molecule-1 (ICAM-1) in high glucose (HG)-cultured glomerular mesangial cells (GMCs). GMCs were transfected with 2 µg of Penter vector or his-PAQR3, respectively. After treatment with HG for 24 h, total proteins were extracted to measure expressions of PAQR3, FN, and ICAM-1 (A,B) . ### P

Techniques Used: Over Expression, Cell Culture, Transfection, Plasmid Preparation

Progestin and adipoQ receptor 3 (PAQR3) depletion reduced the high glucose (HG)-induced fibronectin (FN) and intercellular adhesion molecule-1 (ICAM-1) expressions. Glomerular mesangial cells were transfected with negative control and three pairs of siRNA oligonucleotides targeting PAQR3 for 72 h, and then total proteins were harvested and subjected to Western blot assay. NC is a short form of negative control, and the depletion of β-actin protein acts as a positive control, which is used to evaluate the efficiency of PAQR3 depletion (A,B) . ** P
Figure Legend Snippet: Progestin and adipoQ receptor 3 (PAQR3) depletion reduced the high glucose (HG)-induced fibronectin (FN) and intercellular adhesion molecule-1 (ICAM-1) expressions. Glomerular mesangial cells were transfected with negative control and three pairs of siRNA oligonucleotides targeting PAQR3 for 72 h, and then total proteins were harvested and subjected to Western blot assay. NC is a short form of negative control, and the depletion of β-actin protein acts as a positive control, which is used to evaluate the efficiency of PAQR3 depletion (A,B) . ** P

Techniques Used: Transfection, Negative Control, Western Blot, Positive Control

15) Product Images from "Application of Oxidative Stress to a Tissue-Engineered Vascular Aging Model Induces Endothelial Cell Senescence and Activation"

Article Title: Application of Oxidative Stress to a Tissue-Engineered Vascular Aging Model Induces Endothelial Cell Senescence and Activation

Journal: Cells

doi: 10.3390/cells9051292

H 2 O 2 treatment induced VCAM-1 and E-selectin expression in ECFCs. ( A ) TNF-α increased ICAM-1 expression ( p
Figure Legend Snippet: H 2 O 2 treatment induced VCAM-1 and E-selectin expression in ECFCs. ( A ) TNF-α increased ICAM-1 expression ( p

Techniques Used: Expressing

16) Product Images from "MicroRNA-126 regulates endothelial expression of vascular cell adhesion molecule 1"

Article Title: MicroRNA-126 regulates endothelial expression of vascular cell adhesion molecule 1

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

doi: 10.1073/pnas.0707493105

miR-126 suppresses leukocyte adhesion ex vivo . ( A ) HUVEC were transfected with premiR-126 or a control oligonucleotide for 2 days and then treated with TNF-α or control for 6 h. BCECF-AM-labeled leukocytes were added to the HUVEC, incubated at 37°C for 45 min, and then washed. Adherent cells were photographed with a fluorescent camera. ( B ) HUVEC were transfected with premiR-126 or a control oligonucleotide for 2 days and then treated with TNF-α or control for 6 h. HRP-labeled leukocytes were added to HUVEC, incubated at 37°C for 45 min, and then washed. Adherent cells were lysed, and HRP was assayed by a spectrophotometer at A 450 , and then calibrated to a standard curve ( n = 2 ± SD; P = 0.1 for 0 vs. 30 nM premiR-126). ( C ) HUVEC were transfected with premiR-126 or a control oligonucleotide for 2 days and then treated with TNF-α or control for 6 h. Cell lysates were immunoblotted with antibody to VCAM-1. ( D ) HUVEC were transfected with AS-miR-126 or an AS-control oligonucleotide for 2 days and then treated with TNF-α or control for 6 h. HRP-labeled leukocytes were added to the HUVEC, incubated at 37°C for 45 min, and then washed. Adherent cells were lysed, and HRP was assayed by a spectrophotometer at A 450 and calibrated to a standard curve ( n = 3 ± SD; *, P = 0.02 for 0 vs. 30 nM AS-miR-126). ( E ) HUVEC were transfected with AS-miR-126 or a control oligonucleotide for 2 days and then treated with TNF-α or control for 6 h. Cell lysates were immunoblotted with antibody to VCAM-1. ( F ) HUVEC were treated with TNF-α or control for 6 h. HUVEC were incubated with antibody to VCAM-1, ICAM-1, or control IgG for 30 min at 37°C. HRP-labeled leukocytes were then added to the HUVEC, incubated at 37°C for 45 min, and washed. Adherent cells were lysed, and HRP was assayed by a spectrophotometer at A 450 and calibrated to a standard curve ( n = 3 ± SD; *, P
Figure Legend Snippet: miR-126 suppresses leukocyte adhesion ex vivo . ( A ) HUVEC were transfected with premiR-126 or a control oligonucleotide for 2 days and then treated with TNF-α or control for 6 h. BCECF-AM-labeled leukocytes were added to the HUVEC, incubated at 37°C for 45 min, and then washed. Adherent cells were photographed with a fluorescent camera. ( B ) HUVEC were transfected with premiR-126 or a control oligonucleotide for 2 days and then treated with TNF-α or control for 6 h. HRP-labeled leukocytes were added to HUVEC, incubated at 37°C for 45 min, and then washed. Adherent cells were lysed, and HRP was assayed by a spectrophotometer at A 450 , and then calibrated to a standard curve ( n = 2 ± SD; P = 0.1 for 0 vs. 30 nM premiR-126). ( C ) HUVEC were transfected with premiR-126 or a control oligonucleotide for 2 days and then treated with TNF-α or control for 6 h. Cell lysates were immunoblotted with antibody to VCAM-1. ( D ) HUVEC were transfected with AS-miR-126 or an AS-control oligonucleotide for 2 days and then treated with TNF-α or control for 6 h. HRP-labeled leukocytes were added to the HUVEC, incubated at 37°C for 45 min, and then washed. Adherent cells were lysed, and HRP was assayed by a spectrophotometer at A 450 and calibrated to a standard curve ( n = 3 ± SD; *, P = 0.02 for 0 vs. 30 nM AS-miR-126). ( E ) HUVEC were transfected with AS-miR-126 or a control oligonucleotide for 2 days and then treated with TNF-α or control for 6 h. Cell lysates were immunoblotted with antibody to VCAM-1. ( F ) HUVEC were treated with TNF-α or control for 6 h. HUVEC were incubated with antibody to VCAM-1, ICAM-1, or control IgG for 30 min at 37°C. HRP-labeled leukocytes were then added to the HUVEC, incubated at 37°C for 45 min, and washed. Adherent cells were lysed, and HRP was assayed by a spectrophotometer at A 450 and calibrated to a standard curve ( n = 3 ± SD; *, P

Techniques Used: Ex Vivo, Transfection, Labeling, Incubation, Spectrophotometry

17) Product Images from "G Protein-Coupled Receptor Ca2+-Linked Mitochondrial Reactive Oxygen Species Are Essential for Endothelial/Leukocyte Adherence ▿-Linked Mitochondrial Reactive Oxygen Species Are Essential for Endothelial/Leukocyte Adherence ▿ †"

Article Title: G Protein-Coupled Receptor Ca2+-Linked Mitochondrial Reactive Oxygen Species Are Essential for Endothelial/Leukocyte Adherence ▿-Linked Mitochondrial Reactive Oxygen Species Are Essential for Endothelial/Leukocyte Adherence ▿ †

Journal: Molecular and Cellular Biology

doi: 10.1128/MCB.00493-07

Thrombin-mediated mROS is requisite for leukocyte firm adherence via ICAM-1. Cell Tracker Red-labeled HPMVECs were treated with thrombin (500 mU/ml) or TNF-α (10 ng/ml) with or without MnTBAP (50 μM) pretreatment. An equivalent number of Cell Tracker Green-labeled J774.1 macrophages were added to HPMVECs for each experiment and subjected to simulated circulation to assess leukocyte firm adhesion. (A) Live cell images were acquired under high-power field via confocal microscopy prior to and following 6 min of 2.5 dynes/cm 2 shear stress. (B) Quantitation of adherent leukocytes following thrombin or TNF-α challenge in the absence or presence of MnTBAP. Thrombin-mediated leukocyte/EC binding was effectively reduced by MnTBAP, overexpression of MnSOD, and an anti-ICAM-1 blocking antibody. (C) Proposed model of local versus global leukocyte/EC firm adhesion following GPCR-linked mROS production and TNFR signaling, respectively.
Figure Legend Snippet: Thrombin-mediated mROS is requisite for leukocyte firm adherence via ICAM-1. Cell Tracker Red-labeled HPMVECs were treated with thrombin (500 mU/ml) or TNF-α (10 ng/ml) with or without MnTBAP (50 μM) pretreatment. An equivalent number of Cell Tracker Green-labeled J774.1 macrophages were added to HPMVECs for each experiment and subjected to simulated circulation to assess leukocyte firm adhesion. (A) Live cell images were acquired under high-power field via confocal microscopy prior to and following 6 min of 2.5 dynes/cm 2 shear stress. (B) Quantitation of adherent leukocytes following thrombin or TNF-α challenge in the absence or presence of MnTBAP. Thrombin-mediated leukocyte/EC binding was effectively reduced by MnTBAP, overexpression of MnSOD, and an anti-ICAM-1 blocking antibody. (C) Proposed model of local versus global leukocyte/EC firm adhesion following GPCR-linked mROS production and TNFR signaling, respectively.

Techniques Used: Labeling, Confocal Microscopy, Quantitation Assay, Binding Assay, Over Expression, Blocking Assay

Activation of NF-κB and expression of ICAM-1 by GPCR-linked mROS. (A) Protein binding to the NF-κB consensus sequence following thrombin stimulation in the presence or absence of BAPTA and MnTBAP. (B) NF-κB transcriptional activity in response to thrombin or TNF-α (10 ng/ml) as assessed by luciferase reporter assay. Luciferase reporter constructs were normalized to β-galactosidase activity. (C) Overexpression of MnSOD abolished thrombin-induced NF-κB activity. (D) Global O 2 · − production is assessed by HE fluorescence in response to both thrombin (500 mU/ml) and AA (20 μM) following 10 min of stimulation. (E) Quantitation of nuclear HE fluorescence increase in response to AA and thrombin. (F) VCAM-1 and ICAM-1 expression following thrombin or TNF-α stimulation in the presence of MnTBAP (50 μM), BAPTA (25 μM), or the proteosomal inhibitor MG132 in HPMVECs.
Figure Legend Snippet: Activation of NF-κB and expression of ICAM-1 by GPCR-linked mROS. (A) Protein binding to the NF-κB consensus sequence following thrombin stimulation in the presence or absence of BAPTA and MnTBAP. (B) NF-κB transcriptional activity in response to thrombin or TNF-α (10 ng/ml) as assessed by luciferase reporter assay. Luciferase reporter constructs were normalized to β-galactosidase activity. (C) Overexpression of MnSOD abolished thrombin-induced NF-κB activity. (D) Global O 2 · − production is assessed by HE fluorescence in response to both thrombin (500 mU/ml) and AA (20 μM) following 10 min of stimulation. (E) Quantitation of nuclear HE fluorescence increase in response to AA and thrombin. (F) VCAM-1 and ICAM-1 expression following thrombin or TNF-α stimulation in the presence of MnTBAP (50 μM), BAPTA (25 μM), or the proteosomal inhibitor MG132 in HPMVECs.

Techniques Used: Activation Assay, Expressing, Protein Binding, Sequencing, Activity Assay, Luciferase, Reporter Assay, Construct, Over Expression, Fluorescence, Quantitation Assay

18) Product Images from "G Protein-Coupled Receptor Ca2+-Linked Mitochondrial Reactive Oxygen Species Are Essential for Endothelial/Leukocyte Adherence ▿-Linked Mitochondrial Reactive Oxygen Species Are Essential for Endothelial/Leukocyte Adherence ▿ †"

Article Title: G Protein-Coupled Receptor Ca2+-Linked Mitochondrial Reactive Oxygen Species Are Essential for Endothelial/Leukocyte Adherence ▿-Linked Mitochondrial Reactive Oxygen Species Are Essential for Endothelial/Leukocyte Adherence ▿ †

Journal: Molecular and Cellular Biology

doi: 10.1128/MCB.00493-07

Thrombin-mediated mROS is requisite for leukocyte firm adherence via ICAM-1. Cell Tracker Red-labeled HPMVECs were treated with thrombin (500 mU/ml) or TNF-α (10 ng/ml) with or without MnTBAP (50 μM) pretreatment. An equivalent number of Cell Tracker Green-labeled J774.1 macrophages were added to HPMVECs for each experiment and subjected to simulated circulation to assess leukocyte firm adhesion. (A) Live cell images were acquired under high-power field via confocal microscopy prior to and following 6 min of 2.5 dynes/cm 2 shear stress. (B) Quantitation of adherent leukocytes following thrombin or TNF-α challenge in the absence or presence of MnTBAP. Thrombin-mediated leukocyte/EC binding was effectively reduced by MnTBAP, overexpression of MnSOD, and an anti-ICAM-1 blocking antibody. (C) Proposed model of local versus global leukocyte/EC firm adhesion following GPCR-linked mROS production and TNFR signaling, respectively.
Figure Legend Snippet: Thrombin-mediated mROS is requisite for leukocyte firm adherence via ICAM-1. Cell Tracker Red-labeled HPMVECs were treated with thrombin (500 mU/ml) or TNF-α (10 ng/ml) with or without MnTBAP (50 μM) pretreatment. An equivalent number of Cell Tracker Green-labeled J774.1 macrophages were added to HPMVECs for each experiment and subjected to simulated circulation to assess leukocyte firm adhesion. (A) Live cell images were acquired under high-power field via confocal microscopy prior to and following 6 min of 2.5 dynes/cm 2 shear stress. (B) Quantitation of adherent leukocytes following thrombin or TNF-α challenge in the absence or presence of MnTBAP. Thrombin-mediated leukocyte/EC binding was effectively reduced by MnTBAP, overexpression of MnSOD, and an anti-ICAM-1 blocking antibody. (C) Proposed model of local versus global leukocyte/EC firm adhesion following GPCR-linked mROS production and TNFR signaling, respectively.

Techniques Used: Labeling, Confocal Microscopy, Quantitation Assay, Binding Assay, Over Expression, Blocking Assay

Activation of NF-κB and expression of ICAM-1 by GPCR-linked mROS. (A) Protein binding to the NF-κB consensus sequence following thrombin stimulation in the presence or absence of BAPTA and MnTBAP. (B) NF-κB transcriptional activity in response to thrombin or TNF-α (10 ng/ml) as assessed by luciferase reporter assay. Luciferase reporter constructs were normalized to β-galactosidase activity. (C) Overexpression of MnSOD abolished thrombin-induced NF-κB activity. (D) Global O 2 · − production is assessed by HE fluorescence in response to both thrombin (500 mU/ml) and AA (20 μM) following 10 min of stimulation. (E) Quantitation of nuclear HE fluorescence increase in response to AA and thrombin. (F) VCAM-1 and ICAM-1 expression following thrombin or TNF-α stimulation in the presence of MnTBAP (50 μM), BAPTA (25 μM), or the proteosomal inhibitor MG132 in HPMVECs.
Figure Legend Snippet: Activation of NF-κB and expression of ICAM-1 by GPCR-linked mROS. (A) Protein binding to the NF-κB consensus sequence following thrombin stimulation in the presence or absence of BAPTA and MnTBAP. (B) NF-κB transcriptional activity in response to thrombin or TNF-α (10 ng/ml) as assessed by luciferase reporter assay. Luciferase reporter constructs were normalized to β-galactosidase activity. (C) Overexpression of MnSOD abolished thrombin-induced NF-κB activity. (D) Global O 2 · − production is assessed by HE fluorescence in response to both thrombin (500 mU/ml) and AA (20 μM) following 10 min of stimulation. (E) Quantitation of nuclear HE fluorescence increase in response to AA and thrombin. (F) VCAM-1 and ICAM-1 expression following thrombin or TNF-α stimulation in the presence of MnTBAP (50 μM), BAPTA (25 μM), or the proteosomal inhibitor MG132 in HPMVECs.

Techniques Used: Activation Assay, Expressing, Protein Binding, Sequencing, Activity Assay, Luciferase, Reporter Assay, Construct, Over Expression, Fluorescence, Quantitation Assay

19) Product Images from "Gut Bacteria Drive Kupffer Cell Expansion via MAMP-Mediated ICAM-1 Induction on Sinusoidal Endothelium and Influence Preservation-Reperfusion Injury after Orthotopic Liver Transplantation"

Article Title: Gut Bacteria Drive Kupffer Cell Expansion via MAMP-Mediated ICAM-1 Induction on Sinusoidal Endothelium and Influence Preservation-Reperfusion Injury after Orthotopic Liver Transplantation

Journal: The American Journal of Pathology

doi: 10.1016/j.ajpath.2012.09.010

Constitutive ICAM-1 expression by LSECs is induced by the gut microbiota and permits KC repopulation. A : ICAM-1 (red) and LYVE-1 (green) expression on LSECs [DAPI (blue nuclear stain)]. Original magnification, ×10 (representative images of liver section); ×30 (representative images of portal/central regions). Quantification of immunofluorescence area per high-power field revealed significantly higher ICAM-1 and LYVE-1 expression in CL mice ( n = 3 in the CL group; n = 3 in the GF group). Five fields per region per mouse for a total of 15 images per group were used for analysis. *** P
Figure Legend Snippet: Constitutive ICAM-1 expression by LSECs is induced by the gut microbiota and permits KC repopulation. A : ICAM-1 (red) and LYVE-1 (green) expression on LSECs [DAPI (blue nuclear stain)]. Original magnification, ×10 (representative images of liver section); ×30 (representative images of portal/central regions). Quantification of immunofluorescence area per high-power field revealed significantly higher ICAM-1 and LYVE-1 expression in CL mice ( n = 3 in the CL group; n = 3 in the GF group). Five fields per region per mouse for a total of 15 images per group were used for analysis. *** P

Techniques Used: Expressing, Staining, Immunofluorescence, Mouse Assay

20) Product Images from "Activation of Cannabioid Receptor 2 Attenuates Leukocyte-Endothelial Interactions and Blood-Brain Barrier Dysfunction under Inflammatory Conditions"

Article Title: Activation of Cannabioid Receptor 2 Attenuates Leukocyte-Endothelial Interactions and Blood-Brain Barrier Dysfunction under Inflammatory Conditions

Journal: The Journal of Neuroscience

doi: 10.1523/JNEUROSCI.4628-11.2012

Inhibition of ICAM-1 and VCAM-1 expression by CB2R agonist in activated brain endothelium Immunofluorescence histology was performed on frozen brain tissue sections (15 microns thick) from animals treated as indicated. The sections were stained with DAPI and immunolabeled for ICAM-1. Representative images at 20X (scale bar = 100 microns) and 100X (scale bar = 25 microns) objective power are shown. Sections from animals with LPS-associated encephalitis displayed a high level of immunopositive staining for ICAM-1 in the vasculature (arrows) compared to the marginally positive staining in the control animals (middle and top panels respectively). Sections from animals where simultaneous introduction of O-1966 and LPS was used showed similar levels of ICAM-1 as the untreated control (lower pane). (B) Brain microvessels were isolated and western blots for ICAM-1, PCAM-1 and β-actin were performed. Corresponding densitometry results are shown as the fold change from the untreated control (Mean ± SD). (C) Adhesion assays performed with primary human BMVEC and primary human monocytes as described in the Methods. BMVEC were exposed to TNFα (20 ng/ml) alone or with increasing concentrations of 1μM-50μM of either CB2R agonist JWH133 or O-1966. BMVEC were treated for 4 hrs and the treatments removed prior to the addition of monocytes. The data are represented as fold difference (mean ± SEM) of adhesion, which is the number of adherent cells from the treated condition divided by the basal adhesion in untreated cells. All data collected were from at least three different BMVEC donors and performed in triplicate. (C) Representative histograms of FACS analyses of adhesion molecules ICAM-1 and VCAM-1 on brain endothelial cells after TNFα (20 ng/ml) or LPS (50 ng/ml) exposure with the presence of CB2R agonist O-1966. TNFα and LPS induced a similar surface expression of ICAM-1 and VCAM-1 after 4 hrs exposure. The up regulation of adhesion molecules induced by TNFα or LPS was suppressed by O-1966. The data are represented as the mean fluorescence intensity (MFI) of ICAM-1 or VCAM-1 as a percent of the maximum intensity.
Figure Legend Snippet: Inhibition of ICAM-1 and VCAM-1 expression by CB2R agonist in activated brain endothelium Immunofluorescence histology was performed on frozen brain tissue sections (15 microns thick) from animals treated as indicated. The sections were stained with DAPI and immunolabeled for ICAM-1. Representative images at 20X (scale bar = 100 microns) and 100X (scale bar = 25 microns) objective power are shown. Sections from animals with LPS-associated encephalitis displayed a high level of immunopositive staining for ICAM-1 in the vasculature (arrows) compared to the marginally positive staining in the control animals (middle and top panels respectively). Sections from animals where simultaneous introduction of O-1966 and LPS was used showed similar levels of ICAM-1 as the untreated control (lower pane). (B) Brain microvessels were isolated and western blots for ICAM-1, PCAM-1 and β-actin were performed. Corresponding densitometry results are shown as the fold change from the untreated control (Mean ± SD). (C) Adhesion assays performed with primary human BMVEC and primary human monocytes as described in the Methods. BMVEC were exposed to TNFα (20 ng/ml) alone or with increasing concentrations of 1μM-50μM of either CB2R agonist JWH133 or O-1966. BMVEC were treated for 4 hrs and the treatments removed prior to the addition of monocytes. The data are represented as fold difference (mean ± SEM) of adhesion, which is the number of adherent cells from the treated condition divided by the basal adhesion in untreated cells. All data collected were from at least three different BMVEC donors and performed in triplicate. (C) Representative histograms of FACS analyses of adhesion molecules ICAM-1 and VCAM-1 on brain endothelial cells after TNFα (20 ng/ml) or LPS (50 ng/ml) exposure with the presence of CB2R agonist O-1966. TNFα and LPS induced a similar surface expression of ICAM-1 and VCAM-1 after 4 hrs exposure. The up regulation of adhesion molecules induced by TNFα or LPS was suppressed by O-1966. The data are represented as the mean fluorescence intensity (MFI) of ICAM-1 or VCAM-1 as a percent of the maximum intensity.

Techniques Used: Inhibition, Expressing, Immunofluorescence, Staining, Immunolabeling, Isolation, Western Blot, FACS, Fluorescence

21) Product Images from "Pigment Epithelium-Derived Factor Inhibits Retinal Microvascular Dysfunction Induced By 12/15-Lipoxygenase-Derived Eicosanoids"

Article Title: Pigment Epithelium-Derived Factor Inhibits Retinal Microvascular Dysfunction Induced By 12/15-Lipoxygenase-Derived Eicosanoids

Journal: Biochimica et biophysica acta

doi: 10.1016/j.bbalip.2014.12.017

Anti-inflammatory effect of PEDF on 12-HETE-induced retinal inflammation evaluated by Western blot analysis for VCAM-1 and ICAM-1 Normal C57BL/6J mice were injected intravitreally with vehicle control or 12-HETE with/without PEDF. The animals were sacrificed one week later, and retinas were dissected and prepared for Western blot analysis. A and B) Western blot and densitometric analysis of retinal expression of VCAM-1 and ICAM-1, respectively. VCAM-1 or ICAM-1 intensity relative to the actin for groups injected with 12-HETE with/without PEDF were quantified as percentage of vehicle injected group. Data shown are representative of 4–6 mice studied in each group.
Figure Legend Snippet: Anti-inflammatory effect of PEDF on 12-HETE-induced retinal inflammation evaluated by Western blot analysis for VCAM-1 and ICAM-1 Normal C57BL/6J mice were injected intravitreally with vehicle control or 12-HETE with/without PEDF. The animals were sacrificed one week later, and retinas were dissected and prepared for Western blot analysis. A and B) Western blot and densitometric analysis of retinal expression of VCAM-1 and ICAM-1, respectively. VCAM-1 or ICAM-1 intensity relative to the actin for groups injected with 12-HETE with/without PEDF were quantified as percentage of vehicle injected group. Data shown are representative of 4–6 mice studied in each group.

Techniques Used: Western Blot, Mouse Assay, Injection, Expressing

22) Product Images from "MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1"

Article Title: MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1

Journal: Drug Design, Development and Therapy

doi: 10.2147/DDDT.S188095

The expression of ICAM-1 on the surface of mouse PMVECs. Notes: The mice were euthanized 24 hours after administration of LPS or PBS, and then the lung cells were collected. ( A ) PMVECs were labeled with the antibodies CD31+ and CD45-, and then the expression was assessed using a flow cytometer. ( B ) ICAM-1 was labeled with the antibody against CD54+. ( C ) The expression of ICAM-1 on the membranes of mouse PMVECs was higher in the LPS group than in the other groups. The values presented are the mean ± SEM (n=15 in each group). Comparisons were made by one-way ANOVA, and the results are representative of three independent experiments (* P
Figure Legend Snippet: The expression of ICAM-1 on the surface of mouse PMVECs. Notes: The mice were euthanized 24 hours after administration of LPS or PBS, and then the lung cells were collected. ( A ) PMVECs were labeled with the antibodies CD31+ and CD45-, and then the expression was assessed using a flow cytometer. ( B ) ICAM-1 was labeled with the antibody against CD54+. ( C ) The expression of ICAM-1 on the membranes of mouse PMVECs was higher in the LPS group than in the other groups. The values presented are the mean ± SEM (n=15 in each group). Comparisons were made by one-way ANOVA, and the results are representative of three independent experiments (* P

Techniques Used: Expressing, Mouse Assay, Labeling, Flow Cytometry, Cytometry

A simplified model of the molecular pathway. Notes: Upon stimulation by LPS, the p38 MAPK pathway is activated, and this is followed by the activation of MK2. MMI-0100 is able to inhibit the activation of p-MK2 and reduce the expression of ICAM-1. Abbreviations: LPS, lipopolysaccharides; p-MK2, phosphorylated MK2.
Figure Legend Snippet: A simplified model of the molecular pathway. Notes: Upon stimulation by LPS, the p38 MAPK pathway is activated, and this is followed by the activation of MK2. MMI-0100 is able to inhibit the activation of p-MK2 and reduce the expression of ICAM-1. Abbreviations: LPS, lipopolysaccharides; p-MK2, phosphorylated MK2.

Techniques Used: Activation Assay, Expressing

ICAM-1 expression in mice. Notes: After euthanasia, the lung cells were collected and stained with CD45-PE-labeled and CD31-APC-labeled antibodies for 30 minutes at 25°C. The mouse lung microvascular endothelial cells were collected using CD45- and CD31+ immunomagnetic beads. ( A ) mRNA expression of ICAM-1 in PMVECs was increased significantly in the LPS group. The values presented are mean ± SEM. (n=15 in each group). Comparisons were made by one-way ANOVA, * P
Figure Legend Snippet: ICAM-1 expression in mice. Notes: After euthanasia, the lung cells were collected and stained with CD45-PE-labeled and CD31-APC-labeled antibodies for 30 minutes at 25°C. The mouse lung microvascular endothelial cells were collected using CD45- and CD31+ immunomagnetic beads. ( A ) mRNA expression of ICAM-1 in PMVECs was increased significantly in the LPS group. The values presented are mean ± SEM. (n=15 in each group). Comparisons were made by one-way ANOVA, * P

Techniques Used: Expressing, Mouse Assay, Staining, Labeling

23) Product Images from "MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1"

Article Title: MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1

Journal: Drug Design, Development and Therapy

doi: 10.2147/DDDT.S188095

The expression of ICAM-1 on the surface of mouse PMVECs. Notes: The mice were euthanized 24 hours after administration of LPS or PBS, and then the lung cells were collected. ( A ) PMVECs were labeled with the antibodies CD31+ and CD45-, and then the expression was assessed using a flow cytometer. ( B ) ICAM-1 was labeled with the antibody against CD54+. ( C ) The expression of ICAM-1 on the membranes of mouse PMVECs was higher in the LPS group than in the other groups. The values presented are the mean ± SEM (n=15 in each group). Comparisons were made by one-way ANOVA, and the results are representative of three independent experiments (* P
Figure Legend Snippet: The expression of ICAM-1 on the surface of mouse PMVECs. Notes: The mice were euthanized 24 hours after administration of LPS or PBS, and then the lung cells were collected. ( A ) PMVECs were labeled with the antibodies CD31+ and CD45-, and then the expression was assessed using a flow cytometer. ( B ) ICAM-1 was labeled with the antibody against CD54+. ( C ) The expression of ICAM-1 on the membranes of mouse PMVECs was higher in the LPS group than in the other groups. The values presented are the mean ± SEM (n=15 in each group). Comparisons were made by one-way ANOVA, and the results are representative of three independent experiments (* P

Techniques Used: Expressing, Mouse Assay, Labeling, Flow Cytometry, Cytometry

A simplified model of the molecular pathway. Notes: Upon stimulation by LPS, the p38 MAPK pathway is activated, and this is followed by the activation of MK2. MMI-0100 is able to inhibit the activation of p-MK2 and reduce the expression of ICAM-1. Abbreviations: LPS, lipopolysaccharides; p-MK2, phosphorylated MK2.
Figure Legend Snippet: A simplified model of the molecular pathway. Notes: Upon stimulation by LPS, the p38 MAPK pathway is activated, and this is followed by the activation of MK2. MMI-0100 is able to inhibit the activation of p-MK2 and reduce the expression of ICAM-1. Abbreviations: LPS, lipopolysaccharides; p-MK2, phosphorylated MK2.

Techniques Used: Activation Assay, Expressing

ICAM-1 expression in mice. Notes: After euthanasia, the lung cells were collected and stained with CD45-PE-labeled and CD31-APC-labeled antibodies for 30 minutes at 25°C. The mouse lung microvascular endothelial cells were collected using CD45- and CD31+ immunomagnetic beads. ( A ) mRNA expression of ICAM-1 in PMVECs was increased significantly in the LPS group. The values presented are mean ± SEM. (n=15 in each group). Comparisons were made by one-way ANOVA, * P
Figure Legend Snippet: ICAM-1 expression in mice. Notes: After euthanasia, the lung cells were collected and stained with CD45-PE-labeled and CD31-APC-labeled antibodies for 30 minutes at 25°C. The mouse lung microvascular endothelial cells were collected using CD45- and CD31+ immunomagnetic beads. ( A ) mRNA expression of ICAM-1 in PMVECs was increased significantly in the LPS group. The values presented are mean ± SEM. (n=15 in each group). Comparisons were made by one-way ANOVA, * P

Techniques Used: Expressing, Mouse Assay, Staining, Labeling

24) Product Images from "A critical role of the Gas6-Mer axis in endothelial dysfunction contributing to TA-TMA associated with GVHD"

Article Title: A critical role of the Gas6-Mer axis in endothelial dysfunction contributing to TA-TMA associated with GVHD

Journal: Blood Advances

doi: 10.1182/bloodadvances.2019000222

Effect of Mer inhibition on ICAM-1 and VCAM-1 upregulation induced by exogenous Gas6 or the exposure of sera isolated from patients with grade III aGVHD in ECs. (A,D) The expression of ICAM-1 and VCAM-1 in ECs was upregulated by exogenous Gas6. The ECs were incubated for 24 hours with exogenous Gas6 (0, 100, 200, 400 ng/mL), followed by western blotting. Representative data are from 4 independent experiments. * P
Figure Legend Snippet: Effect of Mer inhibition on ICAM-1 and VCAM-1 upregulation induced by exogenous Gas6 or the exposure of sera isolated from patients with grade III aGVHD in ECs. (A,D) The expression of ICAM-1 and VCAM-1 in ECs was upregulated by exogenous Gas6. The ECs were incubated for 24 hours with exogenous Gas6 (0, 100, 200, 400 ng/mL), followed by western blotting. Representative data are from 4 independent experiments. * P

Techniques Used: Inhibition, Isolation, Expressing, Incubation, Western Blot

25) Product Images from "M?ller Cell-Derived VEGF Is Essential for Diabetes-Induced Retinal Inflammation and Vascular Leakage"

Article Title: M?ller Cell-Derived VEGF Is Essential for Diabetes-Induced Retinal Inflammation and Vascular Leakage

Journal: Diabetes

doi: 10.2337/db09-1420

Analysis of retinal inflammation in conditional VEGF KO mice 2 months after inducing diabetes. A and B : FITC-conjugated ConA staining for adherent leukocytes ( arrows ) in retinal microvasculatures of diabetic conditional VEGF KO mice and WT controls. Scale bar represents 100 μm. C : Quantification of adherent leukocytes in retinal vasculatures of diabetic conditional VEGF KO mice and WT controls. D and E : Immunoblotting analysis of ICAM-1 ( D ) and TNF-α ( E ) expression in conditional VEGF KO mice. F : Immunoblotting analysis of NF-κB p65 phosphorylation in diabetic retinas of conditional VEGF KO mice. Error bar: SEM. *** P
Figure Legend Snippet: Analysis of retinal inflammation in conditional VEGF KO mice 2 months after inducing diabetes. A and B : FITC-conjugated ConA staining for adherent leukocytes ( arrows ) in retinal microvasculatures of diabetic conditional VEGF KO mice and WT controls. Scale bar represents 100 μm. C : Quantification of adherent leukocytes in retinal vasculatures of diabetic conditional VEGF KO mice and WT controls. D and E : Immunoblotting analysis of ICAM-1 ( D ) and TNF-α ( E ) expression in conditional VEGF KO mice. F : Immunoblotting analysis of NF-κB p65 phosphorylation in diabetic retinas of conditional VEGF KO mice. Error bar: SEM. *** P

Techniques Used: Mouse Assay, Staining, Expressing

26) Product Images from "Evidence for the Use of Multiple Mechanisms by Herpes Simplex Virus-1 R7020 to Inhibit Intimal Hyperplasia"

Article Title: Evidence for the Use of Multiple Mechanisms by Herpes Simplex Virus-1 R7020 to Inhibit Intimal Hyperplasia

Journal: PLoS ONE

doi: 10.1371/journal.pone.0130264

Vascular SMCs infected with R7020 form syncytia in vitro . R7020 (1 MOI) infected (R7020) and non-infected (Con) SMCs were cultured for 24 h. Non-infected (TNF-α) and infected cells (TNF-α + R7020) were also cultured in the presence of TNF-α. DIC, DAPI, ICP22 labeled, and ICAM-1 labeled images are shown in rows 1, 2, 3 and 4, respectively with an overlay of all four channels in row 5.
Figure Legend Snippet: Vascular SMCs infected with R7020 form syncytia in vitro . R7020 (1 MOI) infected (R7020) and non-infected (Con) SMCs were cultured for 24 h. Non-infected (TNF-α) and infected cells (TNF-α + R7020) were also cultured in the presence of TNF-α. DIC, DAPI, ICP22 labeled, and ICAM-1 labeled images are shown in rows 1, 2, 3 and 4, respectively with an overlay of all four channels in row 5.

Techniques Used: Infection, In Vitro, Cell Culture, Labeling

27) Product Images from "Neutrophil Adhesion on Endothelial Cells in a Novel Asymmetric Stenosis Model: Effect of Wall Shear Stress Gradients"

Article Title: Neutrophil Adhesion on Endothelial Cells in a Novel Asymmetric Stenosis Model: Effect of Wall Shear Stress Gradients

Journal: Annals of biomedical engineering

doi: 10.1007/s10439-010-0032-4

Preshearing effect on the expression of cell adhesion molecules by non stimulated and TNF-α stimulated HAECs. (A) ICAM-1 and (B) VCAM-1.
Figure Legend Snippet: Preshearing effect on the expression of cell adhesion molecules by non stimulated and TNF-α stimulated HAECs. (A) ICAM-1 and (B) VCAM-1.

Techniques Used: Expressing

Endothelial cell adhesion molecules expression. (A) Confocal images showing endothelial cell upregulation of ICAM-1 and VCAM-1 upon stimulation with TNF-α. (B) Western blotting results showing the dependency in time for ICAM-1 and VCAM-1 upregulation due to TNF-α using β-actin as a loading control.
Figure Legend Snippet: Endothelial cell adhesion molecules expression. (A) Confocal images showing endothelial cell upregulation of ICAM-1 and VCAM-1 upon stimulation with TNF-α. (B) Western blotting results showing the dependency in time for ICAM-1 and VCAM-1 upregulation due to TNF-α using β-actin as a loading control.

Techniques Used: Expressing, Western Blot

Expression of cell adhesion molecules ICAM-1 and VCAM-1 following exposure to TNF-α as observed using confocal microscopy. Initial levels after 24 hrs of TNF-α stimulation are shown, along with the expression after TNF-α was removed for 1 hr, under static conditions, low (1.25 dyne/cm 2 ) and high (6.25 dynes/cm 2 ) wall shear stresses.
Figure Legend Snippet: Expression of cell adhesion molecules ICAM-1 and VCAM-1 following exposure to TNF-α as observed using confocal microscopy. Initial levels after 24 hrs of TNF-α stimulation are shown, along with the expression after TNF-α was removed for 1 hr, under static conditions, low (1.25 dyne/cm 2 ) and high (6.25 dynes/cm 2 ) wall shear stresses.

Techniques Used: Expressing, Confocal Microscopy

Regional expression of cell adhesion molecules ICAM-1 and VCAM-1 in HAECs following exposure to TNF-α for 24 hrs grown in static conditions and after the adhesion assays, which were performed at low shear (1.25 dyne/cm 2 ) for 1 hr, as observed using confocal microscopy.
Figure Legend Snippet: Regional expression of cell adhesion molecules ICAM-1 and VCAM-1 in HAECs following exposure to TNF-α for 24 hrs grown in static conditions and after the adhesion assays, which were performed at low shear (1.25 dyne/cm 2 ) for 1 hr, as observed using confocal microscopy.

Techniques Used: Expressing, Confocal Microscopy

Regional expression of cell adhesion molecules ICAM-1 and VCAM-1 following exposure to TNF-α for presheared cells during 24 hrs and after the adhesion assays at low shear (1.25 dyne/cm 2 ) for 1 hr, as observed using confocal microscopy.
Figure Legend Snippet: Regional expression of cell adhesion molecules ICAM-1 and VCAM-1 following exposure to TNF-α for presheared cells during 24 hrs and after the adhesion assays at low shear (1.25 dyne/cm 2 ) for 1 hr, as observed using confocal microscopy.

Techniques Used: Expressing, Confocal Microscopy

28) Product Images from "Kaempferol modulates pro-inflammatory NF-?B activation by suppressing advanced glycation endproducts-induced NADPH oxidase"

Article Title: Kaempferol modulates pro-inflammatory NF-?B activation by suppressing advanced glycation endproducts-induced NADPH oxidase

Journal: Age

doi: 10.1007/s11357-009-9124-1

Inhibition of NF-κB-dependant gene expression by kaempferol in aged rat. To determine NF-κB-dependent genes and adhesion molecule expressions with age, expressions of MMP-9, MCP-1, RANTES, VCAM-1, and ICAM-1 were examined. As shown in this data, MMP-9, MCP-1, RANTES, VCAM-1, and ICAM-1 levels increased with age, but kaempferol reduced these levels with age. # p
Figure Legend Snippet: Inhibition of NF-κB-dependant gene expression by kaempferol in aged rat. To determine NF-κB-dependent genes and adhesion molecule expressions with age, expressions of MMP-9, MCP-1, RANTES, VCAM-1, and ICAM-1 were examined. As shown in this data, MMP-9, MCP-1, RANTES, VCAM-1, and ICAM-1 levels increased with age, but kaempferol reduced these levels with age. # p

Techniques Used: Inhibition, Expressing

29) Product Images from "Pharmacological inhibition of soluble epoxide hydrolase prevents renal interstitial fibrogenesis in obstructive nephropathy"

Article Title: Pharmacological inhibition of soluble epoxide hydrolase prevents renal interstitial fibrogenesis in obstructive nephropathy

Journal: American Journal of Physiology - Renal Physiology

doi: 10.1152/ajprenal.00531.2014

sEH inhibition reduces inflammatory gene expression during UUO. A : level of keratinocyte chemoattractant (KC), macrophage inflammatory protein (MIP)-2, and monocyte chemotactic protein (MCP)-1 in kidneys in vehicle- or t -TUCB-treated mice after sham operation or UUO using a multiplex immunoassay. B : protein expression of p-p65, TNF-α, and ICAM-1 in kidneys using Western blot analysis. Bands were quantified using Lab Works analysis software. Values are means ± SD; n = 6. # P
Figure Legend Snippet: sEH inhibition reduces inflammatory gene expression during UUO. A : level of keratinocyte chemoattractant (KC), macrophage inflammatory protein (MIP)-2, and monocyte chemotactic protein (MCP)-1 in kidneys in vehicle- or t -TUCB-treated mice after sham operation or UUO using a multiplex immunoassay. B : protein expression of p-p65, TNF-α, and ICAM-1 in kidneys using Western blot analysis. Bands were quantified using Lab Works analysis software. Values are means ± SD; n = 6. # P

Techniques Used: Inhibition, Expressing, Mouse Assay, Multiplex Assay, Western Blot, Software

30) Product Images from "MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1"

Article Title: MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1

Journal: Drug Design, Development and Therapy

doi: 10.2147/DDDT.S188095

The expression of ICAM-1 on the surface of mouse PMVECs. Notes: The mice were euthanized 24 hours after administration of LPS or PBS, and then the lung cells were collected. ( A ) PMVECs were labeled with the antibodies CD31+ and CD45-, and then the expression was assessed using a flow cytometer. ( B ) ICAM-1 was labeled with the antibody against CD54+. ( C ) The expression of ICAM-1 on the membranes of mouse PMVECs was higher in the LPS group than in the other groups. The values presented are the mean ± SEM (n=15 in each group). Comparisons were made by one-way ANOVA, and the results are representative of three independent experiments (* P
Figure Legend Snippet: The expression of ICAM-1 on the surface of mouse PMVECs. Notes: The mice were euthanized 24 hours after administration of LPS or PBS, and then the lung cells were collected. ( A ) PMVECs were labeled with the antibodies CD31+ and CD45-, and then the expression was assessed using a flow cytometer. ( B ) ICAM-1 was labeled with the antibody against CD54+. ( C ) The expression of ICAM-1 on the membranes of mouse PMVECs was higher in the LPS group than in the other groups. The values presented are the mean ± SEM (n=15 in each group). Comparisons were made by one-way ANOVA, and the results are representative of three independent experiments (* P

Techniques Used: Expressing, Mouse Assay, Labeling, Flow Cytometry, Cytometry

A simplified model of the molecular pathway. Notes: Upon stimulation by LPS, the p38 MAPK pathway is activated, and this is followed by the activation of MK2. MMI-0100 is able to inhibit the activation of p-MK2 and reduce the expression of ICAM-1. Abbreviations: LPS, lipopolysaccharides; p-MK2, phosphorylated MK2.
Figure Legend Snippet: A simplified model of the molecular pathway. Notes: Upon stimulation by LPS, the p38 MAPK pathway is activated, and this is followed by the activation of MK2. MMI-0100 is able to inhibit the activation of p-MK2 and reduce the expression of ICAM-1. Abbreviations: LPS, lipopolysaccharides; p-MK2, phosphorylated MK2.

Techniques Used: Activation Assay, Expressing

ICAM-1 expression in mice. Notes: After euthanasia, the lung cells were collected and stained with CD45-PE-labeled and CD31-APC-labeled antibodies for 30 minutes at 25°C. The mouse lung microvascular endothelial cells were collected using CD45- and CD31+ immunomagnetic beads. ( A ) mRNA expression of ICAM-1 in PMVECs was increased significantly in the LPS group. The values presented are mean ± SEM. (n=15 in each group). Comparisons were made by one-way ANOVA, * P
Figure Legend Snippet: ICAM-1 expression in mice. Notes: After euthanasia, the lung cells were collected and stained with CD45-PE-labeled and CD31-APC-labeled antibodies for 30 minutes at 25°C. The mouse lung microvascular endothelial cells were collected using CD45- and CD31+ immunomagnetic beads. ( A ) mRNA expression of ICAM-1 in PMVECs was increased significantly in the LPS group. The values presented are mean ± SEM. (n=15 in each group). Comparisons were made by one-way ANOVA, * P

Techniques Used: Expressing, Mouse Assay, Staining, Labeling

31) Product Images from "MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1"

Article Title: MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1

Journal: Drug Design, Development and Therapy

doi: 10.2147/DDDT.S188095

The expression of ICAM-1 on the surface of mouse PMVECs. Notes: The mice were euthanized 24 hours after administration of LPS or PBS, and then the lung cells were collected. ( A ) PMVECs were labeled with the antibodies CD31+ and CD45-, and then the expression was assessed using a flow cytometer. ( B ) ICAM-1 was labeled with the antibody against CD54+. ( C ) The expression of ICAM-1 on the membranes of mouse PMVECs was higher in the LPS group than in the other groups. The values presented are the mean ± SEM (n=15 in each group). Comparisons were made by one-way ANOVA, and the results are representative of three independent experiments (* P
Figure Legend Snippet: The expression of ICAM-1 on the surface of mouse PMVECs. Notes: The mice were euthanized 24 hours after administration of LPS or PBS, and then the lung cells were collected. ( A ) PMVECs were labeled with the antibodies CD31+ and CD45-, and then the expression was assessed using a flow cytometer. ( B ) ICAM-1 was labeled with the antibody against CD54+. ( C ) The expression of ICAM-1 on the membranes of mouse PMVECs was higher in the LPS group than in the other groups. The values presented are the mean ± SEM (n=15 in each group). Comparisons were made by one-way ANOVA, and the results are representative of three independent experiments (* P

Techniques Used: Expressing, Mouse Assay, Labeling, Flow Cytometry, Cytometry

A simplified model of the molecular pathway. Notes: Upon stimulation by LPS, the p38 MAPK pathway is activated, and this is followed by the activation of MK2. MMI-0100 is able to inhibit the activation of p-MK2 and reduce the expression of ICAM-1. Abbreviations: LPS, lipopolysaccharides; p-MK2, phosphorylated MK2.
Figure Legend Snippet: A simplified model of the molecular pathway. Notes: Upon stimulation by LPS, the p38 MAPK pathway is activated, and this is followed by the activation of MK2. MMI-0100 is able to inhibit the activation of p-MK2 and reduce the expression of ICAM-1. Abbreviations: LPS, lipopolysaccharides; p-MK2, phosphorylated MK2.

Techniques Used: Activation Assay, Expressing

ICAM-1 expression in mice. Notes: After euthanasia, the lung cells were collected and stained with CD45-PE-labeled and CD31-APC-labeled antibodies for 30 minutes at 25°C. The mouse lung microvascular endothelial cells were collected using CD45- and CD31+ immunomagnetic beads. ( A ) mRNA expression of ICAM-1 in PMVECs was increased significantly in the LPS group. The values presented are mean ± SEM. (n=15 in each group). Comparisons were made by one-way ANOVA, * P
Figure Legend Snippet: ICAM-1 expression in mice. Notes: After euthanasia, the lung cells were collected and stained with CD45-PE-labeled and CD31-APC-labeled antibodies for 30 minutes at 25°C. The mouse lung microvascular endothelial cells were collected using CD45- and CD31+ immunomagnetic beads. ( A ) mRNA expression of ICAM-1 in PMVECs was increased significantly in the LPS group. The values presented are mean ± SEM. (n=15 in each group). Comparisons were made by one-way ANOVA, * P

Techniques Used: Expressing, Mouse Assay, Staining, Labeling

32) Product Images from "MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1"

Article Title: MMI-0100 ameliorates lung inflammation in a mouse model of acute respiratory distress syndrome by reducing endothelial expression of ICAM-1

Journal: Drug Design, Development and Therapy

doi: 10.2147/DDDT.S188095

The expression of ICAM-1 on the surface of mouse PMVECs. Notes: The mice were euthanized 24 hours after administration of LPS or PBS, and then the lung cells were collected. ( A ) PMVECs were labeled with the antibodies CD31+ and CD45-, and then the expression was assessed using a flow cytometer. ( B ) ICAM-1 was labeled with the antibody against CD54+. ( C ) The expression of ICAM-1 on the membranes of mouse PMVECs was higher in the LPS group than in the other groups. The values presented are the mean ± SEM (n=15 in each group). Comparisons were made by one-way ANOVA, and the results are representative of three independent experiments (* P
Figure Legend Snippet: The expression of ICAM-1 on the surface of mouse PMVECs. Notes: The mice were euthanized 24 hours after administration of LPS or PBS, and then the lung cells were collected. ( A ) PMVECs were labeled with the antibodies CD31+ and CD45-, and then the expression was assessed using a flow cytometer. ( B ) ICAM-1 was labeled with the antibody against CD54+. ( C ) The expression of ICAM-1 on the membranes of mouse PMVECs was higher in the LPS group than in the other groups. The values presented are the mean ± SEM (n=15 in each group). Comparisons were made by one-way ANOVA, and the results are representative of three independent experiments (* P

Techniques Used: Expressing, Mouse Assay, Labeling, Flow Cytometry, Cytometry

A simplified model of the molecular pathway. Notes: Upon stimulation by LPS, the p38 MAPK pathway is activated, and this is followed by the activation of MK2. MMI-0100 is able to inhibit the activation of p-MK2 and reduce the expression of ICAM-1. Abbreviations: LPS, lipopolysaccharides; p-MK2, phosphorylated MK2.
Figure Legend Snippet: A simplified model of the molecular pathway. Notes: Upon stimulation by LPS, the p38 MAPK pathway is activated, and this is followed by the activation of MK2. MMI-0100 is able to inhibit the activation of p-MK2 and reduce the expression of ICAM-1. Abbreviations: LPS, lipopolysaccharides; p-MK2, phosphorylated MK2.

Techniques Used: Activation Assay, Expressing

ICAM-1 expression in mice. Notes: After euthanasia, the lung cells were collected and stained with CD45-PE-labeled and CD31-APC-labeled antibodies for 30 minutes at 25°C. The mouse lung microvascular endothelial cells were collected using CD45- and CD31+ immunomagnetic beads. ( A ) mRNA expression of ICAM-1 in PMVECs was increased significantly in the LPS group. The values presented are mean ± SEM. (n=15 in each group). Comparisons were made by one-way ANOVA, * P
Figure Legend Snippet: ICAM-1 expression in mice. Notes: After euthanasia, the lung cells were collected and stained with CD45-PE-labeled and CD31-APC-labeled antibodies for 30 minutes at 25°C. The mouse lung microvascular endothelial cells were collected using CD45- and CD31+ immunomagnetic beads. ( A ) mRNA expression of ICAM-1 in PMVECs was increased significantly in the LPS group. The values presented are mean ± SEM. (n=15 in each group). Comparisons were made by one-way ANOVA, * P

Techniques Used: Expressing, Mouse Assay, Staining, Labeling

33) Product Images from "The Effects of Portulaca oleracea on Hypoxia-Induced Pulmonary Edema in Mice"

Article Title: The Effects of Portulaca oleracea on Hypoxia-Induced Pulmonary Edema in Mice

Journal: High Altitude Medicine & Biology

doi: 10.1089/ham.2013.1081

Western blot analysis of ICAM-1, VCAM-1, and P-selectin; (a) is the results of Western blot; (b) , (c) , and (d) are ICAM-1, VCAM-1, and P-selectin relative expression after hypoxia exposure. Con, control; hyp, hypoxia; L, H, hypoxia+H EEPO; hypoxia+L EEPO; M, hypoxia+M EEPO; # p
Figure Legend Snippet: Western blot analysis of ICAM-1, VCAM-1, and P-selectin; (a) is the results of Western blot; (b) , (c) , and (d) are ICAM-1, VCAM-1, and P-selectin relative expression after hypoxia exposure. Con, control; hyp, hypoxia; L, H, hypoxia+H EEPO; hypoxia+L EEPO; M, hypoxia+M EEPO; # p

Techniques Used: Western Blot, Expressing

34) Product Images from "In vivo imaging of endothelial cell adhesion molecule expression after radiosurgery in an animal model of arteriovenous malformation"

Article Title: In vivo imaging of endothelial cell adhesion molecule expression after radiosurgery in an animal model of arteriovenous malformation

Journal: PLoS ONE

doi: 10.1371/journal.pone.0185393

Time course of ICAM-1 and VCAM-1 expression in the rat AVM model. Xenolight-750 probe binding was examined over a period of 84 days for ICAM-1 (A) and VCAM-1 (B) in control and irradiated (15 Gy) animals (n = 7 per group). Raw MFI (mean fluorescence intensity) was normalized to day 1 in matched animals to reduce inter-animal variation. No significant differences were detected at any time between irradiated and control AVMs. Ex vivo image analysis of Xenolight 750-ICAM-1 (C) and Xenolight 750-VCAM-1 (D) probe binding in excised tissue: common carotid artery (CCA), external jugular vein (EJV) (n = 7).
Figure Legend Snippet: Time course of ICAM-1 and VCAM-1 expression in the rat AVM model. Xenolight-750 probe binding was examined over a period of 84 days for ICAM-1 (A) and VCAM-1 (B) in control and irradiated (15 Gy) animals (n = 7 per group). Raw MFI (mean fluorescence intensity) was normalized to day 1 in matched animals to reduce inter-animal variation. No significant differences were detected at any time between irradiated and control AVMs. Ex vivo image analysis of Xenolight 750-ICAM-1 (C) and Xenolight 750-VCAM-1 (D) probe binding in excised tissue: common carotid artery (CCA), external jugular vein (EJV) (n = 7).

Techniques Used: Expressing, Binding Assay, Irradiation, Fluorescence, Ex Vivo

ELISA and immunocytochemical analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. ELISA analysis of surface ICAM-1 (A) and VCAM-1 (D) expression in irradiated bEnd.3 cells normalized to Janus green absorbance to account for changes in cell number. Immunocytochemistry was performed on bEnd.3 cells using CF555-conjugated ICAM-1 or CF640-conjugated VCAM-1 antibodies (red). Staining was quantitated as integrated density using Image J (arbitrary units) for ICAM-1 (B) and VCAM-1 (E). Representative images are shown at 120 h (ICAM-1) (C) or 72 h (VCAM-1) (F) post-radiation at doses of 0–25 Gy. Isotype controls for ICAM-1 (IgG1-CF555) and VCAM-1 (IgG2b-CF640) showed no staining (representative images shown at 25 Gy, 72h). Cells were counterstained with DAPI to visualize nuclei (blue). All images were acquired at a magnification of 200× (scale bar = 100 μm). Values are mean ± SEM, n = 3 for each group.
Figure Legend Snippet: ELISA and immunocytochemical analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. ELISA analysis of surface ICAM-1 (A) and VCAM-1 (D) expression in irradiated bEnd.3 cells normalized to Janus green absorbance to account for changes in cell number. Immunocytochemistry was performed on bEnd.3 cells using CF555-conjugated ICAM-1 or CF640-conjugated VCAM-1 antibodies (red). Staining was quantitated as integrated density using Image J (arbitrary units) for ICAM-1 (B) and VCAM-1 (E). Representative images are shown at 120 h (ICAM-1) (C) or 72 h (VCAM-1) (F) post-radiation at doses of 0–25 Gy. Isotype controls for ICAM-1 (IgG1-CF555) and VCAM-1 (IgG2b-CF640) showed no staining (representative images shown at 25 Gy, 72h). Cells were counterstained with DAPI to visualize nuclei (blue). All images were acquired at a magnification of 200× (scale bar = 100 μm). Values are mean ± SEM, n = 3 for each group.

Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing, Irradiation, Immunocytochemistry, Staining

In vivo near-infrared fluorescence imaging of Xenolight 750 probes in the rat AVM model. Rats with an AVM creation were sham treated or irradiated with a 15 Gy marginal dose to the AVM region by Gamma Knife and imaging performed 12 h after conjugate dye injection (25 μg/kg). Representative montages of x-ray (left), fluorescent (centre) and merged (right) images after injection of Xenolight 750 probes: (A) Xenolight-750 isotype control in irradiated animal; (B) Xenolight 750-ICAM-1 probe and; (C) Xenolight 750-VCAM-1 probe, at day 21 after sham (top panels) or radiation (bottom panels). Image J quantitation of fluorescence at day 21 post-irradiation or sham with Xenolight 750-ICAM-1 (D) or Xenolight 750-VCAM-1 (E) probes and Xenolight-750 isotype control probe.
Figure Legend Snippet: In vivo near-infrared fluorescence imaging of Xenolight 750 probes in the rat AVM model. Rats with an AVM creation were sham treated or irradiated with a 15 Gy marginal dose to the AVM region by Gamma Knife and imaging performed 12 h after conjugate dye injection (25 μg/kg). Representative montages of x-ray (left), fluorescent (centre) and merged (right) images after injection of Xenolight 750 probes: (A) Xenolight-750 isotype control in irradiated animal; (B) Xenolight 750-ICAM-1 probe and; (C) Xenolight 750-VCAM-1 probe, at day 21 after sham (top panels) or radiation (bottom panels). Image J quantitation of fluorescence at day 21 post-irradiation or sham with Xenolight 750-ICAM-1 (D) or Xenolight 750-VCAM-1 (E) probes and Xenolight-750 isotype control probe.

Techniques Used: In Vivo, Fluorescence, Imaging, Irradiation, Injection, Quantitation Assay

Quantitative real-time PCR and western analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. qRT-PCR analysis of ICAM-1 (A) and VCAM-1 (E) gene expression, n = 4 independent experiments. Representative western blots (time course) of ICAM-1 (B) and VCAM-1 (F) protein at 25 Gy. Representative western blots (dose response) of ICAM-1 expression (120 h) (C) and VCAM-1 expression (72 h) (G) post-irradiation. ICAM-1 (D) and VCAM-1 (H) protein expression quantitated using Image J, n = 4. Values are mean ± SEM. Data were normalized to GAPDH (westerns) or HPRT (qRT-PCR).
Figure Legend Snippet: Quantitative real-time PCR and western analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. qRT-PCR analysis of ICAM-1 (A) and VCAM-1 (E) gene expression, n = 4 independent experiments. Representative western blots (time course) of ICAM-1 (B) and VCAM-1 (F) protein at 25 Gy. Representative western blots (dose response) of ICAM-1 expression (120 h) (C) and VCAM-1 expression (72 h) (G) post-irradiation. ICAM-1 (D) and VCAM-1 (H) protein expression quantitated using Image J, n = 4. Values are mean ± SEM. Data were normalized to GAPDH (westerns) or HPRT (qRT-PCR).

Techniques Used: Real-time Polymerase Chain Reaction, Western Blot, Expressing, Irradiation, Quantitative RT-PCR

35) Product Images from "In vivo imaging of endothelial cell adhesion molecule expression after radiosurgery in an animal model of arteriovenous malformation"

Article Title: In vivo imaging of endothelial cell adhesion molecule expression after radiosurgery in an animal model of arteriovenous malformation

Journal: PLoS ONE

doi: 10.1371/journal.pone.0185393

Time course of ICAM-1 and VCAM-1 expression in the rat AVM model. Xenolight-750 probe binding was examined over a period of 84 days for ICAM-1 (A) and VCAM-1 (B) in control and irradiated (15 Gy) animals (n = 7 per group). Raw MFI (mean fluorescence intensity) was normalized to day 1 in matched animals to reduce inter-animal variation. No significant differences were detected at any time between irradiated and control AVMs. Ex vivo image analysis of Xenolight 750-ICAM-1 (C) and Xenolight 750-VCAM-1 (D) probe binding in excised tissue: common carotid artery (CCA), external jugular vein (EJV) (n = 7).
Figure Legend Snippet: Time course of ICAM-1 and VCAM-1 expression in the rat AVM model. Xenolight-750 probe binding was examined over a period of 84 days for ICAM-1 (A) and VCAM-1 (B) in control and irradiated (15 Gy) animals (n = 7 per group). Raw MFI (mean fluorescence intensity) was normalized to day 1 in matched animals to reduce inter-animal variation. No significant differences were detected at any time between irradiated and control AVMs. Ex vivo image analysis of Xenolight 750-ICAM-1 (C) and Xenolight 750-VCAM-1 (D) probe binding in excised tissue: common carotid artery (CCA), external jugular vein (EJV) (n = 7).

Techniques Used: Expressing, Binding Assay, Irradiation, Fluorescence, Ex Vivo

ELISA and immunocytochemical analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. ELISA analysis of surface ICAM-1 (A) and VCAM-1 (D) expression in irradiated bEnd.3 cells normalized to Janus green absorbance to account for changes in cell number. Immunocytochemistry was performed on bEnd.3 cells using CF555-conjugated ICAM-1 or CF640-conjugated VCAM-1 antibodies (red). Staining was quantitated as integrated density using Image J (arbitrary units) for ICAM-1 (B) and VCAM-1 (E). Representative images are shown at 120 h (ICAM-1) (C) or 72 h (VCAM-1) (F) post-radiation at doses of 0–25 Gy. Isotype controls for ICAM-1 (IgG1-CF555) and VCAM-1 (IgG2b-CF640) showed no staining (representative images shown at 25 Gy, 72h). Cells were counterstained with DAPI to visualize nuclei (blue). All images were acquired at a magnification of 200× (scale bar = 100 μm). Values are mean ± SEM, n = 3 for each group.
Figure Legend Snippet: ELISA and immunocytochemical analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. ELISA analysis of surface ICAM-1 (A) and VCAM-1 (D) expression in irradiated bEnd.3 cells normalized to Janus green absorbance to account for changes in cell number. Immunocytochemistry was performed on bEnd.3 cells using CF555-conjugated ICAM-1 or CF640-conjugated VCAM-1 antibodies (red). Staining was quantitated as integrated density using Image J (arbitrary units) for ICAM-1 (B) and VCAM-1 (E). Representative images are shown at 120 h (ICAM-1) (C) or 72 h (VCAM-1) (F) post-radiation at doses of 0–25 Gy. Isotype controls for ICAM-1 (IgG1-CF555) and VCAM-1 (IgG2b-CF640) showed no staining (representative images shown at 25 Gy, 72h). Cells were counterstained with DAPI to visualize nuclei (blue). All images were acquired at a magnification of 200× (scale bar = 100 μm). Values are mean ± SEM, n = 3 for each group.

Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing, Irradiation, Immunocytochemistry, Staining

In vivo near-infrared fluorescence imaging of Xenolight 750 probes in the rat AVM model. Rats with an AVM creation were sham treated or irradiated with a 15 Gy marginal dose to the AVM region by Gamma Knife and imaging performed 12 h after conjugate dye injection (25 μg/kg). Representative montages of x-ray (left), fluorescent (centre) and merged (right) images after injection of Xenolight 750 probes: (A) Xenolight-750 isotype control in irradiated animal; (B) Xenolight 750-ICAM-1 probe and; (C) Xenolight 750-VCAM-1 probe, at day 21 after sham (top panels) or radiation (bottom panels). Image J quantitation of fluorescence at day 21 post-irradiation or sham with Xenolight 750-ICAM-1 (D) or Xenolight 750-VCAM-1 (E) probes and Xenolight-750 isotype control probe.
Figure Legend Snippet: In vivo near-infrared fluorescence imaging of Xenolight 750 probes in the rat AVM model. Rats with an AVM creation were sham treated or irradiated with a 15 Gy marginal dose to the AVM region by Gamma Knife and imaging performed 12 h after conjugate dye injection (25 μg/kg). Representative montages of x-ray (left), fluorescent (centre) and merged (right) images after injection of Xenolight 750 probes: (A) Xenolight-750 isotype control in irradiated animal; (B) Xenolight 750-ICAM-1 probe and; (C) Xenolight 750-VCAM-1 probe, at day 21 after sham (top panels) or radiation (bottom panels). Image J quantitation of fluorescence at day 21 post-irradiation or sham with Xenolight 750-ICAM-1 (D) or Xenolight 750-VCAM-1 (E) probes and Xenolight-750 isotype control probe.

Techniques Used: In Vivo, Fluorescence, Imaging, Irradiation, Injection, Quantitation Assay

Quantitative real-time PCR and western analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. qRT-PCR analysis of ICAM-1 (A) and VCAM-1 (E) gene expression, n = 4 independent experiments. Representative western blots (time course) of ICAM-1 (B) and VCAM-1 (F) protein at 25 Gy. Representative western blots (dose response) of ICAM-1 expression (120 h) (C) and VCAM-1 expression (72 h) (G) post-irradiation. ICAM-1 (D) and VCAM-1 (H) protein expression quantitated using Image J, n = 4. Values are mean ± SEM. Data were normalized to GAPDH (westerns) or HPRT (qRT-PCR).
Figure Legend Snippet: Quantitative real-time PCR and western analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. qRT-PCR analysis of ICAM-1 (A) and VCAM-1 (E) gene expression, n = 4 independent experiments. Representative western blots (time course) of ICAM-1 (B) and VCAM-1 (F) protein at 25 Gy. Representative western blots (dose response) of ICAM-1 expression (120 h) (C) and VCAM-1 expression (72 h) (G) post-irradiation. ICAM-1 (D) and VCAM-1 (H) protein expression quantitated using Image J, n = 4. Values are mean ± SEM. Data were normalized to GAPDH (westerns) or HPRT (qRT-PCR).

Techniques Used: Real-time Polymerase Chain Reaction, Western Blot, Expressing, Irradiation, Quantitative RT-PCR

36) Product Images from "In vivo imaging of endothelial cell adhesion molecule expression after radiosurgery in an animal model of arteriovenous malformation"

Article Title: In vivo imaging of endothelial cell adhesion molecule expression after radiosurgery in an animal model of arteriovenous malformation

Journal: PLoS ONE

doi: 10.1371/journal.pone.0185393

Time course of ICAM-1 and VCAM-1 expression in the rat AVM model. Xenolight-750 probe binding was examined over a period of 84 days for ICAM-1 (A) and VCAM-1 (B) in control and irradiated (15 Gy) animals (n = 7 per group). Raw MFI (mean fluorescence intensity) was normalized to day 1 in matched animals to reduce inter-animal variation. No significant differences were detected at any time between irradiated and control AVMs. Ex vivo image analysis of Xenolight 750-ICAM-1 (C) and Xenolight 750-VCAM-1 (D) probe binding in excised tissue: common carotid artery (CCA), external jugular vein (EJV) (n = 7).
Figure Legend Snippet: Time course of ICAM-1 and VCAM-1 expression in the rat AVM model. Xenolight-750 probe binding was examined over a period of 84 days for ICAM-1 (A) and VCAM-1 (B) in control and irradiated (15 Gy) animals (n = 7 per group). Raw MFI (mean fluorescence intensity) was normalized to day 1 in matched animals to reduce inter-animal variation. No significant differences were detected at any time between irradiated and control AVMs. Ex vivo image analysis of Xenolight 750-ICAM-1 (C) and Xenolight 750-VCAM-1 (D) probe binding in excised tissue: common carotid artery (CCA), external jugular vein (EJV) (n = 7).

Techniques Used: Expressing, Binding Assay, Irradiation, Fluorescence, Ex Vivo

ELISA and immunocytochemical analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. ELISA analysis of surface ICAM-1 (A) and VCAM-1 (D) expression in irradiated bEnd.3 cells normalized to Janus green absorbance to account for changes in cell number. Immunocytochemistry was performed on bEnd.3 cells using CF555-conjugated ICAM-1 or CF640-conjugated VCAM-1 antibodies (red). Staining was quantitated as integrated density using Image J (arbitrary units) for ICAM-1 (B) and VCAM-1 (E). Representative images are shown at 120 h (ICAM-1) (C) or 72 h (VCAM-1) (F) post-radiation at doses of 0–25 Gy. Isotype controls for ICAM-1 (IgG1-CF555) and VCAM-1 (IgG2b-CF640) showed no staining (representative images shown at 25 Gy, 72h). Cells were counterstained with DAPI to visualize nuclei (blue). All images were acquired at a magnification of 200× (scale bar = 100 μm). Values are mean ± SEM, n = 3 for each group.
Figure Legend Snippet: ELISA and immunocytochemical analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. ELISA analysis of surface ICAM-1 (A) and VCAM-1 (D) expression in irradiated bEnd.3 cells normalized to Janus green absorbance to account for changes in cell number. Immunocytochemistry was performed on bEnd.3 cells using CF555-conjugated ICAM-1 or CF640-conjugated VCAM-1 antibodies (red). Staining was quantitated as integrated density using Image J (arbitrary units) for ICAM-1 (B) and VCAM-1 (E). Representative images are shown at 120 h (ICAM-1) (C) or 72 h (VCAM-1) (F) post-radiation at doses of 0–25 Gy. Isotype controls for ICAM-1 (IgG1-CF555) and VCAM-1 (IgG2b-CF640) showed no staining (representative images shown at 25 Gy, 72h). Cells were counterstained with DAPI to visualize nuclei (blue). All images were acquired at a magnification of 200× (scale bar = 100 μm). Values are mean ± SEM, n = 3 for each group.

Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing, Irradiation, Immunocytochemistry, Staining

In vivo near-infrared fluorescence imaging of Xenolight 750 probes in the rat AVM model. Rats with an AVM creation were sham treated or irradiated with a 15 Gy marginal dose to the AVM region by Gamma Knife and imaging performed 12 h after conjugate dye injection (25 μg/kg). Representative montages of x-ray (left), fluorescent (centre) and merged (right) images after injection of Xenolight 750 probes: (A) Xenolight-750 isotype control in irradiated animal; (B) Xenolight 750-ICAM-1 probe and; (C) Xenolight 750-VCAM-1 probe, at day 21 after sham (top panels) or radiation (bottom panels). Image J quantitation of fluorescence at day 21 post-irradiation or sham with Xenolight 750-ICAM-1 (D) or Xenolight 750-VCAM-1 (E) probes and Xenolight-750 isotype control probe.
Figure Legend Snippet: In vivo near-infrared fluorescence imaging of Xenolight 750 probes in the rat AVM model. Rats with an AVM creation were sham treated or irradiated with a 15 Gy marginal dose to the AVM region by Gamma Knife and imaging performed 12 h after conjugate dye injection (25 μg/kg). Representative montages of x-ray (left), fluorescent (centre) and merged (right) images after injection of Xenolight 750 probes: (A) Xenolight-750 isotype control in irradiated animal; (B) Xenolight 750-ICAM-1 probe and; (C) Xenolight 750-VCAM-1 probe, at day 21 after sham (top panels) or radiation (bottom panels). Image J quantitation of fluorescence at day 21 post-irradiation or sham with Xenolight 750-ICAM-1 (D) or Xenolight 750-VCAM-1 (E) probes and Xenolight-750 isotype control probe.

Techniques Used: In Vivo, Fluorescence, Imaging, Irradiation, Injection, Quantitation Assay

Quantitative real-time PCR and western analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. qRT-PCR analysis of ICAM-1 (A) and VCAM-1 (E) gene expression, n = 4 independent experiments. Representative western blots (time course) of ICAM-1 (B) and VCAM-1 (F) protein at 25 Gy. Representative western blots (dose response) of ICAM-1 expression (120 h) (C) and VCAM-1 expression (72 h) (G) post-irradiation. ICAM-1 (D) and VCAM-1 (H) protein expression quantitated using Image J, n = 4. Values are mean ± SEM. Data were normalized to GAPDH (westerns) or HPRT (qRT-PCR).
Figure Legend Snippet: Quantitative real-time PCR and western analysis of ICAM-1 and VCAM-1 expression in irradiated bEnd.3 cells. qRT-PCR analysis of ICAM-1 (A) and VCAM-1 (E) gene expression, n = 4 independent experiments. Representative western blots (time course) of ICAM-1 (B) and VCAM-1 (F) protein at 25 Gy. Representative western blots (dose response) of ICAM-1 expression (120 h) (C) and VCAM-1 expression (72 h) (G) post-irradiation. ICAM-1 (D) and VCAM-1 (H) protein expression quantitated using Image J, n = 4. Values are mean ± SEM. Data were normalized to GAPDH (westerns) or HPRT (qRT-PCR).

Techniques Used: Real-time Polymerase Chain Reaction, Western Blot, Expressing, Irradiation, Quantitative RT-PCR

37) Product Images from "Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow"

Article Title: Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow

Journal: PLoS ONE

doi: 10.1371/journal.pone.0167576

Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.
Figure Legend Snippet: Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.

Techniques Used: Flow Cytometry, Activity Assay, Activation Assay

ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p
Figure Legend Snippet: ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p

Techniques Used: Expressing, Flow Cytometry, Western Blot

38) Product Images from "Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow"

Article Title: Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow

Journal: PLoS ONE

doi: 10.1371/journal.pone.0167576

Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.
Figure Legend Snippet: Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.

Techniques Used: Flow Cytometry, Activity Assay, Activation Assay

ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p
Figure Legend Snippet: ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p

Techniques Used: Expressing, Flow Cytometry, Western Blot

39) Product Images from "Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow"

Article Title: Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow

Journal: PLoS ONE

doi: 10.1371/journal.pone.0167576

Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.
Figure Legend Snippet: Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.

Techniques Used: Flow Cytometry, Activity Assay, Activation Assay

ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p
Figure Legend Snippet: ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p

Techniques Used: Expressing, Flow Cytometry, Western Blot

40) Product Images from "Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow"

Article Title: Glycocalyx Degradation Induces a Proinflammatory Phenotype and Increased Leukocyte Adhesion in Cultured Endothelial Cells under Flow

Journal: PLoS ONE

doi: 10.1371/journal.pone.0167576

Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.
Figure Legend Snippet: Model for the molecular adhesion pathway altered with degradation. Flow diagram illustrating how glycocalyx degradation interrupts the negative feedback loop regulating NF-κB activity. When the glycocalyx is degraded, NO levels are inhibited resulting in increased NF-κB activity. This results in the over-stimulation/activation of ECs evidenced by an increase in ICAM-1 and leukocyte adhesion.

Techniques Used: Flow Cytometry, Activity Assay, Activation Assay

ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p
Figure Legend Snippet: ICAM-1 protein expression with flow and degradation. (A) Representative western blot images showing ICAM-1 with GAPDH as the loading control. (B) Quantification of western blots using densitometry (n = 4, *p

Techniques Used: Expressing, Flow Cytometry, Western Blot

Related Articles

Chick Chorioallantoic Membrane Assay:

Article Title: Reduced immune cell infiltration and increased pro-inflammatory mediators in the brain of Type 2 diabetic mouse model infected with West Nile virus
Article Snippet: .. It has been demonstrated that TMEV infection induces the expression of CAM such as ICAM-1 and VCAM-1 in the mice brain, which plays an important role in mediating the infiltration of leukocytes into the brain [ - ]. .. In our study, significant up-regulation of CAM is observed at day 8 after infection in the brain of WT mice, which correlates with high virus replication (Figure C) [ ].

Infection:

Article Title: Reduced immune cell infiltration and increased pro-inflammatory mediators in the brain of Type 2 diabetic mouse model infected with West Nile virus
Article Snippet: .. Moreover, leukocyte and macrophage infiltrates were decreased in the brains of ICAM-1-/- mice after WNV infection [ ]. .. Similarly, we observed an increased expression of ICAM-1 and E-selectin in the brains of WT mice after WNV infection, which correlates with leukocyte infiltration in these mice (Figures and ).

Article Title: Reduced immune cell infiltration and increased pro-inflammatory mediators in the brain of Type 2 diabetic mouse model infected with West Nile virus
Article Snippet: .. It has been demonstrated that TMEV infection induces the expression of CAM such as ICAM-1 and VCAM-1 in the mice brain, which plays an important role in mediating the infiltration of leukocytes into the brain [ - ]. .. In our study, significant up-regulation of CAM is observed at day 8 after infection in the brain of WT mice, which correlates with high virus replication (Figure C) [ ].

Mouse Assay:

Article Title: Reduced immune cell infiltration and increased pro-inflammatory mediators in the brain of Type 2 diabetic mouse model infected with West Nile virus
Article Snippet: .. Moreover, leukocyte and macrophage infiltrates were decreased in the brains of ICAM-1-/- mice after WNV infection [ ]. .. Similarly, we observed an increased expression of ICAM-1 and E-selectin in the brains of WT mice after WNV infection, which correlates with leukocyte infiltration in these mice (Figures and ).

Article Title: Reduced immune cell infiltration and increased pro-inflammatory mediators in the brain of Type 2 diabetic mouse model infected with West Nile virus
Article Snippet: .. It has been demonstrated that TMEV infection induces the expression of CAM such as ICAM-1 and VCAM-1 in the mice brain, which plays an important role in mediating the infiltration of leukocytes into the brain [ - ]. .. In our study, significant up-regulation of CAM is observed at day 8 after infection in the brain of WT mice, which correlates with high virus replication (Figure C) [ ].

Article Title: Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis
Article Snippet: .. Similarly, in WTD-fed ApoE KO mice, immunofluorescence of the aorta tissues showed that ICAM-1 and ET-1 expression were decreased in rosiglitazone and DYSGT groups compared with ApoE KO group ( ). .. Discussion In the present study, we investigated the protective role of DYSGT in diabetic atherosclerosis using western diet-ApoE KO mice.

other:

Article Title: Expression of Intercellular Adhesion Molecule-1 and E-Selectin in Gastric Cancer and Their Clinical Significance
Article Snippet: Although subgroup analysis was not possible because the sample size of our study was small, we think that there is a significant possibility of ICAM-1 as the independent prognostic factor in gastric cancer, especially in the advanced stage, when a large-scale, multicenter research study will be undertaken.

Article Title: TNF-α augmented Porphyromonas gingivalis invasion in human gingival epithelial cells through Rab5 and ICAM-1
Article Snippet: Antibodies Antibodies were obtained from the following sources: antiserum for P. gingivalis whole cells was kindly donated by Dr. Fuminobu Yoshimura (Aichi-gakuin University, Aichi, Japan); mouse monoclonal antibody specific for ICAM-1, goat polyclonal antibody specific for ICAM-1, mouse monoclonal antibody specific for TNFRI, mouse monoclonal antibody specific for TNFRII and mouse immunoglobulin G (IgG) (R & D Systems, Minneapolis, MN); mouse monoclonal antibody specific for Rab5 (BD Biosciences); rabbit polyclonal antibody specific for ICAM-1 (Santa Cruz Biotechnology, Dallas, TX); goat IgG (Alpha Diagnostic Intl.

Article Title: The involvement of high mobility group 1 cytokine and phospholipases A2 in diabetic retinopathy
Article Snippet: Similarly, TNF-α, VEGF and ICAM-1 were increased at least to 2.5 fold in DR when compared to that of control tissue.

Article Title: Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis
Article Snippet: Adhesion molecules such as VCAM-1 and ICAM-1 play a significant role in the process of atherosclerosis as they ensure the recruitment of inflammatory cells.

Expressing:

Article Title: The 18-kDa Translocator Protein Inhibits Vascular Cell Adhesion Molecule-1 Expression via Inhibition of Mitochondrial Reactive Oxygen Species
Article Snippet: .. As shown by Western blot analysis with anti-VCAM-1 and ICAM-1 in , VCAM-1 and ICAM-1 were minimally detected in the un-stimulated condition, whereas treatment with PMA resulted in a marked increase in VCAM-1 and ICAM-1 expression. .. Adenoviral FLAG-tagged TSPO gene transfer in an MOI range of 10–100 successfully induced TSPO expression, as assessed by Western blot analysis with the anti-TSPO antibody.

Article Title: Reduced immune cell infiltration and increased pro-inflammatory mediators in the brain of Type 2 diabetic mouse model infected with West Nile virus
Article Snippet: .. It has been demonstrated that TMEV infection induces the expression of CAM such as ICAM-1 and VCAM-1 in the mice brain, which plays an important role in mediating the infiltration of leukocytes into the brain [ - ]. .. In our study, significant up-regulation of CAM is observed at day 8 after infection in the brain of WT mice, which correlates with high virus replication (Figure C) [ ].

Article Title: Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis
Article Snippet: .. Similarly, in WTD-fed ApoE KO mice, immunofluorescence of the aorta tissues showed that ICAM-1 and ET-1 expression were decreased in rosiglitazone and DYSGT groups compared with ApoE KO group ( ). .. Discussion In the present study, we investigated the protective role of DYSGT in diabetic atherosclerosis using western diet-ApoE KO mice.

Western Blot:

Article Title: The 18-kDa Translocator Protein Inhibits Vascular Cell Adhesion Molecule-1 Expression via Inhibition of Mitochondrial Reactive Oxygen Species
Article Snippet: .. As shown by Western blot analysis with anti-VCAM-1 and ICAM-1 in , VCAM-1 and ICAM-1 were minimally detected in the un-stimulated condition, whereas treatment with PMA resulted in a marked increase in VCAM-1 and ICAM-1 expression. .. Adenoviral FLAG-tagged TSPO gene transfer in an MOI range of 10–100 successfully induced TSPO expression, as assessed by Western blot analysis with the anti-TSPO antibody.

Immunofluorescence:

Article Title: Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis
Article Snippet: .. Similarly, in WTD-fed ApoE KO mice, immunofluorescence of the aorta tissues showed that ICAM-1 and ET-1 expression were decreased in rosiglitazone and DYSGT groups compared with ApoE KO group ( ). .. Discussion In the present study, we investigated the protective role of DYSGT in diabetic atherosclerosis using western diet-ApoE KO mice.

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  • 93
    Santa Cruz Biotechnology icam 1 mouse monoclonal antibody
    CNF1 affects the cytoadherence of pRBCs by acting on endothelial cells. (A) Dose response experiments for CNF1 effect on P . falciparum viability, assessed by pLDH enzymatic assay. P . falciparum asexual stages were treated with increasing concentrations of CNF1 and epoxomicin as reference drug. Data represent mean ± SEM from at least three experiments. (B) Scanning electron micrographs of pRBCs, untreated (upper panels) and treated with CNF1 (lower panels). Note the production, on the surface of infected erythrocytes, of regularly structured knobs that are not modified (higher magnification, right panels) by the challenge with CNF1. (C) Statistical analysis shows no differences in density of knobs per unit area (knobs/μm 2 ) between CNF1-treated or untreated mature trophozoites (P = 0.89; n = 10). (D) CNF1 was added to HBEC-5i cells either overnight before the adhesion process (pre CNF1) or after the adhesion assay of pRBCs, for 4 or 24 h (post CNF1). Cells were lysed and processed for western blot analysis. The <t>ICAM-1</t> immunoblot showing a representative experiment (upper panel) was normalized as a function of α-tubulin (lower panel) and expressed as arbitrary units (histogram). Note that CNF1 is able to down-regulate ICAM-1 only at 24 h of treatment. Data, expressed as percentage of control (= 1), represent mean ± SEM from at least three independent experiments. * p
    Icam 1 Mouse Monoclonal Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/icam 1 mouse monoclonal antibody/product/Santa Cruz Biotechnology
    Average 93 stars, based on 4 article reviews
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    icam 1 mouse monoclonal antibody - by Bioz Stars, 2020-09
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    91
    Santa Cruz Biotechnology anti icam 1 monoclonal antibody
    <t>ICAM-1</t> expression in endothelial cells that attached to either oxidized or native laminin-1. Bars represent mean value ± standard error of means of at least 15 independent experiments. * indicates significant difference with the value obtained in endothelial cells that attached to non-oxidized laminin-1. ** indicates significant difference with the value obtained in endothelial cells that attached to either oxidized or native laminin-1.
    Anti Icam 1 Monoclonal Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti icam 1 monoclonal antibody/product/Santa Cruz Biotechnology
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti icam 1 monoclonal antibody - by Bioz Stars, 2020-09
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    92
    Santa Cruz Biotechnology icam 1
    Effect of DYSGT on ET-1, <t>ICAM-1,</t> and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P
    Icam 1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 35 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    icam 1 - by Bioz Stars, 2020-09
    92/100 stars
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    Image Search Results


    CNF1 affects the cytoadherence of pRBCs by acting on endothelial cells. (A) Dose response experiments for CNF1 effect on P . falciparum viability, assessed by pLDH enzymatic assay. P . falciparum asexual stages were treated with increasing concentrations of CNF1 and epoxomicin as reference drug. Data represent mean ± SEM from at least three experiments. (B) Scanning electron micrographs of pRBCs, untreated (upper panels) and treated with CNF1 (lower panels). Note the production, on the surface of infected erythrocytes, of regularly structured knobs that are not modified (higher magnification, right panels) by the challenge with CNF1. (C) Statistical analysis shows no differences in density of knobs per unit area (knobs/μm 2 ) between CNF1-treated or untreated mature trophozoites (P = 0.89; n = 10). (D) CNF1 was added to HBEC-5i cells either overnight before the adhesion process (pre CNF1) or after the adhesion assay of pRBCs, for 4 or 24 h (post CNF1). Cells were lysed and processed for western blot analysis. The ICAM-1 immunoblot showing a representative experiment (upper panel) was normalized as a function of α-tubulin (lower panel) and expressed as arbitrary units (histogram). Note that CNF1 is able to down-regulate ICAM-1 only at 24 h of treatment. Data, expressed as percentage of control (= 1), represent mean ± SEM from at least three independent experiments. * p

    Journal: PLoS ONE

    Article Title: The bacterial protein CNF1 as a new strategy against Plasmodium falciparum cytoadherence

    doi: 10.1371/journal.pone.0213529

    Figure Lengend Snippet: CNF1 affects the cytoadherence of pRBCs by acting on endothelial cells. (A) Dose response experiments for CNF1 effect on P . falciparum viability, assessed by pLDH enzymatic assay. P . falciparum asexual stages were treated with increasing concentrations of CNF1 and epoxomicin as reference drug. Data represent mean ± SEM from at least three experiments. (B) Scanning electron micrographs of pRBCs, untreated (upper panels) and treated with CNF1 (lower panels). Note the production, on the surface of infected erythrocytes, of regularly structured knobs that are not modified (higher magnification, right panels) by the challenge with CNF1. (C) Statistical analysis shows no differences in density of knobs per unit area (knobs/μm 2 ) between CNF1-treated or untreated mature trophozoites (P = 0.89; n = 10). (D) CNF1 was added to HBEC-5i cells either overnight before the adhesion process (pre CNF1) or after the adhesion assay of pRBCs, for 4 or 24 h (post CNF1). Cells were lysed and processed for western blot analysis. The ICAM-1 immunoblot showing a representative experiment (upper panel) was normalized as a function of α-tubulin (lower panel) and expressed as arbitrary units (histogram). Note that CNF1 is able to down-regulate ICAM-1 only at 24 h of treatment. Data, expressed as percentage of control (= 1), represent mean ± SEM from at least three independent experiments. * p

    Article Snippet: Then, cells were incubated with ICAM-1 mouse monoclonal antibody (1 μg per 1x106 cells) (Santa Cruz Biotechnology, INC, Dallas, Texas, USA) for 30 min at 4°C, washed with cold PBS, and then incubated with secondary Alexa 488 goat anti-mouse IgG (1:100; Molecular Probes, USA) antibody for 30 min at 4°C.

    Techniques: Enzymatic Assay, Infection, Modification, Cell Adhesion Assay, Western Blot

    ICAM-1 expression in endothelial cells that attached to either oxidized or native laminin-1. Bars represent mean value ± standard error of means of at least 15 independent experiments. * indicates significant difference with the value obtained in endothelial cells that attached to non-oxidized laminin-1. ** indicates significant difference with the value obtained in endothelial cells that attached to either oxidized or native laminin-1.

    Journal: International Journal of Experimental Pathology

    Article Title: Oxidized laminin-1 induces increased monocyte attachment and expression of ICAM-1 in endothelial cells

    doi: 10.1111/j.1365-2613.2009.00686.x

    Figure Lengend Snippet: ICAM-1 expression in endothelial cells that attached to either oxidized or native laminin-1. Bars represent mean value ± standard error of means of at least 15 independent experiments. * indicates significant difference with the value obtained in endothelial cells that attached to non-oxidized laminin-1. ** indicates significant difference with the value obtained in endothelial cells that attached to either oxidized or native laminin-1.

    Article Snippet: Anti-ICAM-1 monoclonal antibody [Mouse anti-human IgG1, epitope FL (h)] was purchased from Santa Cruz Biotechnology, Inc (Heidelberg, Germany).

    Techniques: Expressing

    Effect of DYSGT on ET-1, ICAM-1, and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis

    doi: 10.1155/2013/783576

    Figure Lengend Snippet: Effect of DYSGT on ET-1, ICAM-1, and PPAR- γ protein expression in the aorta of ApoE KO mice. Western blots and corresponding densitometric analyses of ET-1, ICAM-1, and PPAR- γ in aortic tissue. Values are expressed as mean ± S.E. ( n = 4); ** P

    Article Snippet: Similarly, in WTD-fed ApoE KO mice, immunofluorescence of the aorta tissues showed that ICAM-1 and ET-1 expression were decreased in rosiglitazone and DYSGT groups compared with ApoE KO group ( ).

    Techniques: Expressing, Mouse Assay, Western Blot

    Immunofluorescence staining of (a) ICAM-1 and (b) ET-1 in the aorta. Representative histological sections are thoracic aorta of Cont., ApoE KO mice, ApoE mice treated with rosiglitazone, and ApoE mice treated with DYSGT incubated with anti-ICAM-1, anti-ET-1 antibodies, respectively. Original magnification: 100x.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis

    doi: 10.1155/2013/783576

    Figure Lengend Snippet: Immunofluorescence staining of (a) ICAM-1 and (b) ET-1 in the aorta. Representative histological sections are thoracic aorta of Cont., ApoE KO mice, ApoE mice treated with rosiglitazone, and ApoE mice treated with DYSGT incubated with anti-ICAM-1, anti-ET-1 antibodies, respectively. Original magnification: 100x.

    Article Snippet: Similarly, in WTD-fed ApoE KO mice, immunofluorescence of the aorta tissues showed that ICAM-1 and ET-1 expression were decreased in rosiglitazone and DYSGT groups compared with ApoE KO group ( ).

    Techniques: Immunofluorescence, Staining, Mouse Assay, Incubation