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Epigallocatechin gallate inhibits angiotensin II-induced endothelial barrier dysfunction via inhibition of the p38 MAPK/HSP27 pathway.

Yang D, Liu J, Tian C, Zeng Y, Zheng YH, Fang Q, Li HH - Acta Pharmacol. Sin. (2010)

Bottom Line: These effects were abolished by pretreatment with the p38 MAPK inhibitor SB203580 10 μmol/L, indicating that the Ang II-induced endothelial barrier dysfunction was via activation of the p38 MAPK/HSP27 pathway.Furthermore, treatment with EGCG (5-25) μmol/L inhibited Ang II-induced activation of the p38 MAPK/HSP27 pathway, thereby reducing endothelial stress fiber formation and hyperpermeability.Our data demonstrate that EGCG inhibits Ang II-induced endothelial stress fiber formation and hyperpermeability via inactivation of p38 MAPK/HSP27 pathway, and suggest that EGCG may protect against endothelial barrier dysfunction and injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Capital Medical University, Beijing, China.

ABSTRACT

Aim: To investigate the effect of epigallocatechin gallate (EGCG) on angiotensin II (Ang II)-induced stress fiber formation and hyperpermeability in endothelial cells.

Methods: Human umbilical vein endothelial cells (HUVECs) were treated with Ang II in the absence or presence of EGCG or mitogen-activated protein kinases (MAPKs) inhibitors. The resulting stress fibers were stained with rhodamine-phalloidin and examined using confocal microscopy. The permeability of the endothelium was tested with fluorescein-isothiocyanate labeled bovine serum albumin (FITC-BSA), and the phosphorylation levels of several proteins were determined using Western blot analysis.

Results: Ang II (1-100 nmol/L) treatment markedly provoked stress fiber formation and hyperpermeability in HUVECs in a time- and dose-dependent manner. These effects were abolished by pretreatment with the p38 MAPK inhibitor SB203580 10 μmol/L, indicating that the Ang II-induced endothelial barrier dysfunction was via activation of the p38 MAPK/HSP27 pathway. Furthermore, treatment with EGCG (5-25) μmol/L inhibited Ang II-induced activation of the p38 MAPK/HSP27 pathway, thereby reducing endothelial stress fiber formation and hyperpermeability.

Conclusion: Our data demonstrate that EGCG inhibits Ang II-induced endothelial stress fiber formation and hyperpermeability via inactivation of p38 MAPK/HSP27 pathway, and suggest that EGCG may protect against endothelial barrier dysfunction and injury.

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EGCG suppresses Ang II-induced endothelial stress fiber formation and hyperpermeability. (A) The dose-dependent effect of EGCG on Ang II-induced stress fiber formation. HUVECs were pretreated with 0 to 25 μmol/L of EGCG for 30 min before a 15 min incubation with 100 nmol/L of Ang II. The stress fibers were stained and examined as in Figure 1A (n=3, Bar=20 μm). (B) The dose-dependent effect of EGCG on Ang II-induced endothelial hyperpermeability. HUVECs were pretreated with EGCG as in A prior to a 60 min incubation with 100 nmol/L of Ang II. The endothelial permeability was tested as in Figure 1B. n=4. Mean±SD. bP<0.05 vs untreated cells (control). eP<0.05 vs Ang II-treated cells.
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fig3: EGCG suppresses Ang II-induced endothelial stress fiber formation and hyperpermeability. (A) The dose-dependent effect of EGCG on Ang II-induced stress fiber formation. HUVECs were pretreated with 0 to 25 μmol/L of EGCG for 30 min before a 15 min incubation with 100 nmol/L of Ang II. The stress fibers were stained and examined as in Figure 1A (n=3, Bar=20 μm). (B) The dose-dependent effect of EGCG on Ang II-induced endothelial hyperpermeability. HUVECs were pretreated with EGCG as in A prior to a 60 min incubation with 100 nmol/L of Ang II. The endothelial permeability was tested as in Figure 1B. n=4. Mean±SD. bP<0.05 vs untreated cells (control). eP<0.05 vs Ang II-treated cells.

Mentions: EGCG, which is the major catechin derived from green tea, is associated with a reduced risk of cardiovascular disease11. Thus, we wanted to determine if EGCG affects Ang II-induced endothelial stress fiber formation and hyperpermeability. The HUVECs were pretreated with 0 to 25 μmol/L of EGCG for 30 min and subsequently stimulated with 100 nmol/L of Ang II. As shown in Figure 3A and 3B, EGCG attenuated Ang II-induced endothelial stress fiber formation and hyperpermeability in a dose-dependent manner, and there was complete inhibition with 25 μmol/L of Ang II. These results demonstrate that EGCG protects against Ang II-induced endothelial barrier dysfunction.


Epigallocatechin gallate inhibits angiotensin II-induced endothelial barrier dysfunction via inhibition of the p38 MAPK/HSP27 pathway.

Yang D, Liu J, Tian C, Zeng Y, Zheng YH, Fang Q, Li HH - Acta Pharmacol. Sin. (2010)

EGCG suppresses Ang II-induced endothelial stress fiber formation and hyperpermeability. (A) The dose-dependent effect of EGCG on Ang II-induced stress fiber formation. HUVECs were pretreated with 0 to 25 μmol/L of EGCG for 30 min before a 15 min incubation with 100 nmol/L of Ang II. The stress fibers were stained and examined as in Figure 1A (n=3, Bar=20 μm). (B) The dose-dependent effect of EGCG on Ang II-induced endothelial hyperpermeability. HUVECs were pretreated with EGCG as in A prior to a 60 min incubation with 100 nmol/L of Ang II. The endothelial permeability was tested as in Figure 1B. n=4. Mean±SD. bP<0.05 vs untreated cells (control). eP<0.05 vs Ang II-treated cells.
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4012900&req=5

fig3: EGCG suppresses Ang II-induced endothelial stress fiber formation and hyperpermeability. (A) The dose-dependent effect of EGCG on Ang II-induced stress fiber formation. HUVECs were pretreated with 0 to 25 μmol/L of EGCG for 30 min before a 15 min incubation with 100 nmol/L of Ang II. The stress fibers were stained and examined as in Figure 1A (n=3, Bar=20 μm). (B) The dose-dependent effect of EGCG on Ang II-induced endothelial hyperpermeability. HUVECs were pretreated with EGCG as in A prior to a 60 min incubation with 100 nmol/L of Ang II. The endothelial permeability was tested as in Figure 1B. n=4. Mean±SD. bP<0.05 vs untreated cells (control). eP<0.05 vs Ang II-treated cells.
Mentions: EGCG, which is the major catechin derived from green tea, is associated with a reduced risk of cardiovascular disease11. Thus, we wanted to determine if EGCG affects Ang II-induced endothelial stress fiber formation and hyperpermeability. The HUVECs were pretreated with 0 to 25 μmol/L of EGCG for 30 min and subsequently stimulated with 100 nmol/L of Ang II. As shown in Figure 3A and 3B, EGCG attenuated Ang II-induced endothelial stress fiber formation and hyperpermeability in a dose-dependent manner, and there was complete inhibition with 25 μmol/L of Ang II. These results demonstrate that EGCG protects against Ang II-induced endothelial barrier dysfunction.

Bottom Line: These effects were abolished by pretreatment with the p38 MAPK inhibitor SB203580 10 μmol/L, indicating that the Ang II-induced endothelial barrier dysfunction was via activation of the p38 MAPK/HSP27 pathway.Furthermore, treatment with EGCG (5-25) μmol/L inhibited Ang II-induced activation of the p38 MAPK/HSP27 pathway, thereby reducing endothelial stress fiber formation and hyperpermeability.Our data demonstrate that EGCG inhibits Ang II-induced endothelial stress fiber formation and hyperpermeability via inactivation of p38 MAPK/HSP27 pathway, and suggest that EGCG may protect against endothelial barrier dysfunction and injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Capital Medical University, Beijing, China.

ABSTRACT

Aim: To investigate the effect of epigallocatechin gallate (EGCG) on angiotensin II (Ang II)-induced stress fiber formation and hyperpermeability in endothelial cells.

Methods: Human umbilical vein endothelial cells (HUVECs) were treated with Ang II in the absence or presence of EGCG or mitogen-activated protein kinases (MAPKs) inhibitors. The resulting stress fibers were stained with rhodamine-phalloidin and examined using confocal microscopy. The permeability of the endothelium was tested with fluorescein-isothiocyanate labeled bovine serum albumin (FITC-BSA), and the phosphorylation levels of several proteins were determined using Western blot analysis.

Results: Ang II (1-100 nmol/L) treatment markedly provoked stress fiber formation and hyperpermeability in HUVECs in a time- and dose-dependent manner. These effects were abolished by pretreatment with the p38 MAPK inhibitor SB203580 10 μmol/L, indicating that the Ang II-induced endothelial barrier dysfunction was via activation of the p38 MAPK/HSP27 pathway. Furthermore, treatment with EGCG (5-25) μmol/L inhibited Ang II-induced activation of the p38 MAPK/HSP27 pathway, thereby reducing endothelial stress fiber formation and hyperpermeability.

Conclusion: Our data demonstrate that EGCG inhibits Ang II-induced endothelial stress fiber formation and hyperpermeability via inactivation of p38 MAPK/HSP27 pathway, and suggest that EGCG may protect against endothelial barrier dysfunction and injury.

Show MeSH
Related in: MedlinePlus