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Gelantis Inc endothelial permeability hcaecs
Effects of eotaxin, antimycin A, MnTBAP, ginkgolide B and CCR3 on <t>endothelial</t> monolayer <t>permeability</t> in <t>HCAECs.</t> Endothelial monolayer permeability was analyzed with a costar transwell system and a Texas Red-labeled dextran tracer. A, Concentration-dependent study. HCAECs were treated with increasing concentrations of eotaxin (50, 100 and 200 ng/mL), TNF-α (2 ng/mL) or with ginkgolide B (5 μM) for 24 h. n=3, *p<0.05 B, Effects of CCR3 receptor blocking and heat-inactivation (HI) of eotaxin on endothelial permeability. HCAECs were treated with eotaxin (100 ng/mL) or HI-eotaxin (100 gm/mL) with or without anti-CCR3 antibody 24 h. n=3, *p<0.05. C, Effect of antimycin A on endothelial permeability. HCAECs were treated with antimycin A (10 μg/mL) for 24 h in the presence or absence of antioxidant MnTBAP (2 μM). n=3, *p<0.05. D, Western blot analysis. HCAECs were treated with eotaxin (100 ng/mL) and/or MnTBAP (2 μM) for 24 h and CCR3 protein levels were determined by Western blot. Loading efficiency was determined by reprobing the blot with β-actin antibody. Experiments were repeated twice. Statistical comparison is indicated by the arrow head. Error bars represent SD.
Endothelial Permeability Hcaecs, supplied by Gelantis Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/endothelial+permeability+hcaecs/pmc02784176-63-0-6?v=Gelantis+Inc
Average 90 stars, based on 1 article reviews
endothelial permeability hcaecs - by Bioz Stars, 2026-07
90/100 stars

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1) Product Images from "Eotaxin Increases Monolayer Permeability of Human Coronary Artery Endothelial Cells"

Article Title: Eotaxin Increases Monolayer Permeability of Human Coronary Artery Endothelial Cells

Journal:

doi: 10.1161/ATVBAHA.109.194134

Effects of eotaxin, antimycin A, MnTBAP, ginkgolide B and CCR3 on endothelial monolayer permeability in HCAECs. Endothelial monolayer permeability was analyzed with a costar transwell system and a Texas Red-labeled dextran tracer. A, Concentration-dependent study. HCAECs were treated with increasing concentrations of eotaxin (50, 100 and 200 ng/mL), TNF-α (2 ng/mL) or with ginkgolide B (5 μM) for 24 h. n=3, *p<0.05 B, Effects of CCR3 receptor blocking and heat-inactivation (HI) of eotaxin on endothelial permeability. HCAECs were treated with eotaxin (100 ng/mL) or HI-eotaxin (100 gm/mL) with or without anti-CCR3 antibody 24 h. n=3, *p<0.05. C, Effect of antimycin A on endothelial permeability. HCAECs were treated with antimycin A (10 μg/mL) for 24 h in the presence or absence of antioxidant MnTBAP (2 μM). n=3, *p<0.05. D, Western blot analysis. HCAECs were treated with eotaxin (100 ng/mL) and/or MnTBAP (2 μM) for 24 h and CCR3 protein levels were determined by Western blot. Loading efficiency was determined by reprobing the blot with β-actin antibody. Experiments were repeated twice. Statistical comparison is indicated by the arrow head. Error bars represent SD.
Figure Legend Snippet: Effects of eotaxin, antimycin A, MnTBAP, ginkgolide B and CCR3 on endothelial monolayer permeability in HCAECs. Endothelial monolayer permeability was analyzed with a costar transwell system and a Texas Red-labeled dextran tracer. A, Concentration-dependent study. HCAECs were treated with increasing concentrations of eotaxin (50, 100 and 200 ng/mL), TNF-α (2 ng/mL) or with ginkgolide B (5 μM) for 24 h. n=3, *p<0.05 B, Effects of CCR3 receptor blocking and heat-inactivation (HI) of eotaxin on endothelial permeability. HCAECs were treated with eotaxin (100 ng/mL) or HI-eotaxin (100 gm/mL) with or without anti-CCR3 antibody 24 h. n=3, *p<0.05. C, Effect of antimycin A on endothelial permeability. HCAECs were treated with antimycin A (10 μg/mL) for 24 h in the presence or absence of antioxidant MnTBAP (2 μM). n=3, *p<0.05. D, Western blot analysis. HCAECs were treated with eotaxin (100 ng/mL) and/or MnTBAP (2 μM) for 24 h and CCR3 protein levels were determined by Western blot. Loading efficiency was determined by reprobing the blot with β-actin antibody. Experiments were repeated twice. Statistical comparison is indicated by the arrow head. Error bars represent SD.

Techniques Used: Permeability, Labeling, Concentration Assay, Blocking Assay, Western Blot, Comparison

Effects of eotaxin on the expression of junctional molecules in HCAECs. HCAECs were treated with serial concentrations of eotaxin (50, 100 and 200 ng/mL) for 24 h. A, The mRNA levels of ZO-1, claudin-1, occludin, JAM-1 and VE cadherin were analyzed by real time PCR, and values were normalized to GAPDH [2(Ct GAPDH −Ct gene of interest)] in each sample. n=3 *p<0.05 (compared with controls). B, The protein levels of ZO-1, occludin, claudin-1, VE cadherin and JAM-1 were analyzed by Western blot analysis. Loading efficiency was determined by reprobing the blot with β-actin antibody. Eotaxin and antioxidant MnTBAP were used. Experiments were repeated twice. C, Histogram of flow cytometry analysis showing protein levels of ZO-1, claudin-1, and occludin under the control and eotaxin-treated conditions. HCAECs were treated with 100 ng/mL eotaxin for 24 h. Experiments were repeated twice.
Figure Legend Snippet: Effects of eotaxin on the expression of junctional molecules in HCAECs. HCAECs were treated with serial concentrations of eotaxin (50, 100 and 200 ng/mL) for 24 h. A, The mRNA levels of ZO-1, claudin-1, occludin, JAM-1 and VE cadherin were analyzed by real time PCR, and values were normalized to GAPDH [2(Ct GAPDH −Ct gene of interest)] in each sample. n=3 *p<0.05 (compared with controls). B, The protein levels of ZO-1, occludin, claudin-1, VE cadherin and JAM-1 were analyzed by Western blot analysis. Loading efficiency was determined by reprobing the blot with β-actin antibody. Eotaxin and antioxidant MnTBAP were used. Experiments were repeated twice. C, Histogram of flow cytometry analysis showing protein levels of ZO-1, claudin-1, and occludin under the control and eotaxin-treated conditions. HCAECs were treated with 100 ng/mL eotaxin for 24 h. Experiments were repeated twice.

Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Western Blot, Flow Cytometry, Control

Time course study of the effect of eotaxin on mRNA levels of tight junction molecules in HCAECs. Cells were treated with eotaxin (100 ng/mL) for different time points (0, 45 min, 2 h, 6 h, 18 h and 24 h) and the mRNA levels of ZO-1 (A), occludin (B) and claudin-1 (C) were determined by real-time PCR and values were normalized to GAPDH [2(Ct GAPDH −Ct gene of interest)] in each sample. n=3, *p<0.05 (compared with controls). Error bars represent SD.
Figure Legend Snippet: Time course study of the effect of eotaxin on mRNA levels of tight junction molecules in HCAECs. Cells were treated with eotaxin (100 ng/mL) for different time points (0, 45 min, 2 h, 6 h, 18 h and 24 h) and the mRNA levels of ZO-1 (A), occludin (B) and claudin-1 (C) were determined by real-time PCR and values were normalized to GAPDH [2(Ct GAPDH −Ct gene of interest)] in each sample. n=3, *p<0.05 (compared with controls). Error bars represent SD.

Techniques Used: Real-time Polymerase Chain Reaction

Effects of eotaxin, antimycin A, TNF-α, and MnTBAP on the cellular glutathione (GSH) levels in HCAECs. Cells were treated with eotaxin (100 ng/mL), antimycin A (10 μg/mL), TNF-α (2 ng/mL) and/or MnTBAP (2 μM) for 45 min. Cellular GSH levels were determined by a GSH-Glo Glutathione assay kit. n=3. *p<005 (the comparison is indicated by the arrow head). Error bars represent SD.
Figure Legend Snippet: Effects of eotaxin, antimycin A, TNF-α, and MnTBAP on the cellular glutathione (GSH) levels in HCAECs. Cells were treated with eotaxin (100 ng/mL), antimycin A (10 μg/mL), TNF-α (2 ng/mL) and/or MnTBAP (2 μM) for 45 min. Cellular GSH levels were determined by a GSH-Glo Glutathione assay kit. n=3. *p<005 (the comparison is indicated by the arrow head). Error bars represent SD.

Techniques Used: Glutathione Assay, Comparison

Effects of eotaxin, antimycin A and MnTBAP on the activation of p38, Stat3 and NFκB in HCAECs. A, Phosphorylation of p38 and Stat3 as well as nuclear translocation of NF-kB p65 in HCAECs. Cells were treated with either eotaxin (100 ng/mL) or antimycin A (10 μg/mL) for 45 min or pretreated with MnTBAP (2 μM) for 30 min followed by antimycin A treatment for 30 min. Cytoplasmic and nuclear extracts were isolated, respectively. Phosphorylated (p) and total p38 and Stat3 as well as NF-kB p65 proteins were detected by the Western blotting analysis. Loading efficiency was determined by reprobing the blot with β-actin antibody. The experiment was repeated twice. B, Endothelial permeability. HCAECs were treated with eotaxin (100 ng/mL) alone or pretreated with specific p38 inhibitor SB203580 followed by eotaxin treatment for 24 h. Endothelial permeability was assayed. n=3. *p<0.05 (the comparison is indicated by the arrow head). Error bars represent SD.
Figure Legend Snippet: Effects of eotaxin, antimycin A and MnTBAP on the activation of p38, Stat3 and NFκB in HCAECs. A, Phosphorylation of p38 and Stat3 as well as nuclear translocation of NF-kB p65 in HCAECs. Cells were treated with either eotaxin (100 ng/mL) or antimycin A (10 μg/mL) for 45 min or pretreated with MnTBAP (2 μM) for 30 min followed by antimycin A treatment for 30 min. Cytoplasmic and nuclear extracts were isolated, respectively. Phosphorylated (p) and total p38 and Stat3 as well as NF-kB p65 proteins were detected by the Western blotting analysis. Loading efficiency was determined by reprobing the blot with β-actin antibody. The experiment was repeated twice. B, Endothelial permeability. HCAECs were treated with eotaxin (100 ng/mL) alone or pretreated with specific p38 inhibitor SB203580 followed by eotaxin treatment for 24 h. Endothelial permeability was assayed. n=3. *p<0.05 (the comparison is indicated by the arrow head). Error bars represent SD.

Techniques Used: Activation Assay, Phospho-proteomics, Translocation Assay, Isolation, Western Blot, Permeability, Comparison



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Gelantis Inc endothelial permeability hcaecs
Effects of eotaxin, antimycin A, MnTBAP, ginkgolide B and CCR3 on <t>endothelial</t> monolayer <t>permeability</t> in <t>HCAECs.</t> Endothelial monolayer permeability was analyzed with a costar transwell system and a Texas Red-labeled dextran tracer. A, Concentration-dependent study. HCAECs were treated with increasing concentrations of eotaxin (50, 100 and 200 ng/mL), TNF-α (2 ng/mL) or with ginkgolide B (5 μM) for 24 h. n=3, *p<0.05 B, Effects of CCR3 receptor blocking and heat-inactivation (HI) of eotaxin on endothelial permeability. HCAECs were treated with eotaxin (100 ng/mL) or HI-eotaxin (100 gm/mL) with or without anti-CCR3 antibody 24 h. n=3, *p<0.05. C, Effect of antimycin A on endothelial permeability. HCAECs were treated with antimycin A (10 μg/mL) for 24 h in the presence or absence of antioxidant MnTBAP (2 μM). n=3, *p<0.05. D, Western blot analysis. HCAECs were treated with eotaxin (100 ng/mL) and/or MnTBAP (2 μM) for 24 h and CCR3 protein levels were determined by Western blot. Loading efficiency was determined by reprobing the blot with β-actin antibody. Experiments were repeated twice. Statistical comparison is indicated by the arrow head. Error bars represent SD.
Endothelial Permeability Hcaecs, supplied by Gelantis Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/endothelial+permeability+hcaecs/pmc02784176-63-0-6?v=Gelantis+Inc
Average 90 stars, based on 1 article reviews
endothelial permeability hcaecs - by Bioz Stars, 2026-07
90/100 stars
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Effects of eotaxin, antimycin A, MnTBAP, ginkgolide B and CCR3 on endothelial monolayer permeability in HCAECs. Endothelial monolayer permeability was analyzed with a costar transwell system and a Texas Red-labeled dextran tracer. A, Concentration-dependent study. HCAECs were treated with increasing concentrations of eotaxin (50, 100 and 200 ng/mL), TNF-α (2 ng/mL) or with ginkgolide B (5 μM) for 24 h. n=3, *p<0.05 B, Effects of CCR3 receptor blocking and heat-inactivation (HI) of eotaxin on endothelial permeability. HCAECs were treated with eotaxin (100 ng/mL) or HI-eotaxin (100 gm/mL) with or without anti-CCR3 antibody 24 h. n=3, *p<0.05. C, Effect of antimycin A on endothelial permeability. HCAECs were treated with antimycin A (10 μg/mL) for 24 h in the presence or absence of antioxidant MnTBAP (2 μM). n=3, *p<0.05. D, Western blot analysis. HCAECs were treated with eotaxin (100 ng/mL) and/or MnTBAP (2 μM) for 24 h and CCR3 protein levels were determined by Western blot. Loading efficiency was determined by reprobing the blot with β-actin antibody. Experiments were repeated twice. Statistical comparison is indicated by the arrow head. Error bars represent SD.

Journal:

Article Title: Eotaxin Increases Monolayer Permeability of Human Coronary Artery Endothelial Cells

doi: 10.1161/ATVBAHA.109.194134

Figure Lengend Snippet: Effects of eotaxin, antimycin A, MnTBAP, ginkgolide B and CCR3 on endothelial monolayer permeability in HCAECs. Endothelial monolayer permeability was analyzed with a costar transwell system and a Texas Red-labeled dextran tracer. A, Concentration-dependent study. HCAECs were treated with increasing concentrations of eotaxin (50, 100 and 200 ng/mL), TNF-α (2 ng/mL) or with ginkgolide B (5 μM) for 24 h. n=3, *p<0.05 B, Effects of CCR3 receptor blocking and heat-inactivation (HI) of eotaxin on endothelial permeability. HCAECs were treated with eotaxin (100 ng/mL) or HI-eotaxin (100 gm/mL) with or without anti-CCR3 antibody 24 h. n=3, *p<0.05. C, Effect of antimycin A on endothelial permeability. HCAECs were treated with antimycin A (10 μg/mL) for 24 h in the presence or absence of antioxidant MnTBAP (2 μM). n=3, *p<0.05. D, Western blot analysis. HCAECs were treated with eotaxin (100 ng/mL) and/or MnTBAP (2 μM) for 24 h and CCR3 protein levels were determined by Western blot. Loading efficiency was determined by reprobing the blot with β-actin antibody. Experiments were repeated twice. Statistical comparison is indicated by the arrow head. Error bars represent SD.

Article Snippet: Endothelial Permeability HCAECs were obtained from Gelantis (San Diego, CA) and cultured in HCAEC Growth medium (Gelantis).

Techniques: Permeability, Labeling, Concentration Assay, Blocking Assay, Western Blot, Comparison

Effects of eotaxin on the expression of junctional molecules in HCAECs. HCAECs were treated with serial concentrations of eotaxin (50, 100 and 200 ng/mL) for 24 h. A, The mRNA levels of ZO-1, claudin-1, occludin, JAM-1 and VE cadherin were analyzed by real time PCR, and values were normalized to GAPDH [2(Ct GAPDH −Ct gene of interest)] in each sample. n=3 *p<0.05 (compared with controls). B, The protein levels of ZO-1, occludin, claudin-1, VE cadherin and JAM-1 were analyzed by Western blot analysis. Loading efficiency was determined by reprobing the blot with β-actin antibody. Eotaxin and antioxidant MnTBAP were used. Experiments were repeated twice. C, Histogram of flow cytometry analysis showing protein levels of ZO-1, claudin-1, and occludin under the control and eotaxin-treated conditions. HCAECs were treated with 100 ng/mL eotaxin for 24 h. Experiments were repeated twice.

Journal:

Article Title: Eotaxin Increases Monolayer Permeability of Human Coronary Artery Endothelial Cells

doi: 10.1161/ATVBAHA.109.194134

Figure Lengend Snippet: Effects of eotaxin on the expression of junctional molecules in HCAECs. HCAECs were treated with serial concentrations of eotaxin (50, 100 and 200 ng/mL) for 24 h. A, The mRNA levels of ZO-1, claudin-1, occludin, JAM-1 and VE cadherin were analyzed by real time PCR, and values were normalized to GAPDH [2(Ct GAPDH −Ct gene of interest)] in each sample. n=3 *p<0.05 (compared with controls). B, The protein levels of ZO-1, occludin, claudin-1, VE cadherin and JAM-1 were analyzed by Western blot analysis. Loading efficiency was determined by reprobing the blot with β-actin antibody. Eotaxin and antioxidant MnTBAP were used. Experiments were repeated twice. C, Histogram of flow cytometry analysis showing protein levels of ZO-1, claudin-1, and occludin under the control and eotaxin-treated conditions. HCAECs were treated with 100 ng/mL eotaxin for 24 h. Experiments were repeated twice.

Article Snippet: Endothelial Permeability HCAECs were obtained from Gelantis (San Diego, CA) and cultured in HCAEC Growth medium (Gelantis).

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

Time course study of the effect of eotaxin on mRNA levels of tight junction molecules in HCAECs. Cells were treated with eotaxin (100 ng/mL) for different time points (0, 45 min, 2 h, 6 h, 18 h and 24 h) and the mRNA levels of ZO-1 (A), occludin (B) and claudin-1 (C) were determined by real-time PCR and values were normalized to GAPDH [2(Ct GAPDH −Ct gene of interest)] in each sample. n=3, *p<0.05 (compared with controls). Error bars represent SD.

Journal:

Article Title: Eotaxin Increases Monolayer Permeability of Human Coronary Artery Endothelial Cells

doi: 10.1161/ATVBAHA.109.194134

Figure Lengend Snippet: Time course study of the effect of eotaxin on mRNA levels of tight junction molecules in HCAECs. Cells were treated with eotaxin (100 ng/mL) for different time points (0, 45 min, 2 h, 6 h, 18 h and 24 h) and the mRNA levels of ZO-1 (A), occludin (B) and claudin-1 (C) were determined by real-time PCR and values were normalized to GAPDH [2(Ct GAPDH −Ct gene of interest)] in each sample. n=3, *p<0.05 (compared with controls). Error bars represent SD.

Article Snippet: Endothelial Permeability HCAECs were obtained from Gelantis (San Diego, CA) and cultured in HCAEC Growth medium (Gelantis).

Techniques: Real-time Polymerase Chain Reaction

Effects of eotaxin, antimycin A, TNF-α, and MnTBAP on the cellular glutathione (GSH) levels in HCAECs. Cells were treated with eotaxin (100 ng/mL), antimycin A (10 μg/mL), TNF-α (2 ng/mL) and/or MnTBAP (2 μM) for 45 min. Cellular GSH levels were determined by a GSH-Glo Glutathione assay kit. n=3. *p<005 (the comparison is indicated by the arrow head). Error bars represent SD.

Journal:

Article Title: Eotaxin Increases Monolayer Permeability of Human Coronary Artery Endothelial Cells

doi: 10.1161/ATVBAHA.109.194134

Figure Lengend Snippet: Effects of eotaxin, antimycin A, TNF-α, and MnTBAP on the cellular glutathione (GSH) levels in HCAECs. Cells were treated with eotaxin (100 ng/mL), antimycin A (10 μg/mL), TNF-α (2 ng/mL) and/or MnTBAP (2 μM) for 45 min. Cellular GSH levels were determined by a GSH-Glo Glutathione assay kit. n=3. *p<005 (the comparison is indicated by the arrow head). Error bars represent SD.

Article Snippet: Endothelial Permeability HCAECs were obtained from Gelantis (San Diego, CA) and cultured in HCAEC Growth medium (Gelantis).

Techniques: Glutathione Assay, Comparison

Effects of eotaxin, antimycin A and MnTBAP on the activation of p38, Stat3 and NFκB in HCAECs. A, Phosphorylation of p38 and Stat3 as well as nuclear translocation of NF-kB p65 in HCAECs. Cells were treated with either eotaxin (100 ng/mL) or antimycin A (10 μg/mL) for 45 min or pretreated with MnTBAP (2 μM) for 30 min followed by antimycin A treatment for 30 min. Cytoplasmic and nuclear extracts were isolated, respectively. Phosphorylated (p) and total p38 and Stat3 as well as NF-kB p65 proteins were detected by the Western blotting analysis. Loading efficiency was determined by reprobing the blot with β-actin antibody. The experiment was repeated twice. B, Endothelial permeability. HCAECs were treated with eotaxin (100 ng/mL) alone or pretreated with specific p38 inhibitor SB203580 followed by eotaxin treatment for 24 h. Endothelial permeability was assayed. n=3. *p<0.05 (the comparison is indicated by the arrow head). Error bars represent SD.

Journal:

Article Title: Eotaxin Increases Monolayer Permeability of Human Coronary Artery Endothelial Cells

doi: 10.1161/ATVBAHA.109.194134

Figure Lengend Snippet: Effects of eotaxin, antimycin A and MnTBAP on the activation of p38, Stat3 and NFκB in HCAECs. A, Phosphorylation of p38 and Stat3 as well as nuclear translocation of NF-kB p65 in HCAECs. Cells were treated with either eotaxin (100 ng/mL) or antimycin A (10 μg/mL) for 45 min or pretreated with MnTBAP (2 μM) for 30 min followed by antimycin A treatment for 30 min. Cytoplasmic and nuclear extracts were isolated, respectively. Phosphorylated (p) and total p38 and Stat3 as well as NF-kB p65 proteins were detected by the Western blotting analysis. Loading efficiency was determined by reprobing the blot with β-actin antibody. The experiment was repeated twice. B, Endothelial permeability. HCAECs were treated with eotaxin (100 ng/mL) alone or pretreated with specific p38 inhibitor SB203580 followed by eotaxin treatment for 24 h. Endothelial permeability was assayed. n=3. *p<0.05 (the comparison is indicated by the arrow head). Error bars represent SD.

Article Snippet: Endothelial Permeability HCAECs were obtained from Gelantis (San Diego, CA) and cultured in HCAEC Growth medium (Gelantis).

Techniques: Activation Assay, Phospho-proteomics, Translocation Assay, Isolation, Western Blot, Permeability, Comparison