2011•Chinese Journal of ArteriosclerosisRequires access

The Effect of Angiotensin(1-7) on Phosphorylation of p38 MAP Kinases Induced by AngiotensinII in Human Umbilical Vein Endothelial Cells

Liang Chang

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Abstract

Aim To study the effect of angiotensin(1-7) on inhibiting the inflammation induced by angiotensinⅡ(AngⅡ).Methods Cultured human umbilical vein endothelial cells(HUVEC) were randomly dividied into different groups,then incubated in the presence of Ang(1-7),AngⅡ and the specific inhibitor of Ang(1-7),A-779,and so on.The phosphorylation of p38MAPK were determined by Western blot,and the mRNA for the mas receptor were determined by reverse transcriptional PCR. Results Ang(1-7) dose-dependently inhibited the phosphorylation of p38MAPK induced by AngⅡ in HUVECs.The expression of p38MAPK phosphorylation died down markedly at 1 000 nmol/L of Ang(1-7).Pre-treatment with A-779 for 10 min in HUVEC before Ang(1-7) and AngⅡ used,the expression of p38 MAPK phosphorylation was nonsignificantly changed. Conclusion Ang(1-7) effectively represses the phosphorylation of p38MAPK induced by AngⅡ in HUVEC.

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Aim To study the effect of angiotensin(1-7) on inhibiting the inflammation induced by angiotensinⅡ(AngⅡ).Methods Cultured human umbilical vein endothelial cells(HUVEC) were randomly dividied into different groups,then incubated in the presence of Ang(1-7),AngⅡ and the specific inhibitor of Ang(1-7),A-779,and so on.The phosphorylation of p38MAPK were determined by Western blot,and the mRNA for the mas receptor were determined by reverse transcriptional PCR. Results Ang(1-7) dose-dependently inhibited the phosphorylation of p38MAPK induced by AngⅡ in HUVECs.The expression of p38MAPK phosphorylation died down markedly at 1 000 nmol/L of Ang(1-7).Pre-treatment with A-779 for 10 min in HUVEC before Ang(1-7) and AngⅡ used,the expression of p38 MAPK phosphorylation was nonsignificantly changed. Conclusion Ang(1-7) effectively represses the phosphorylation of p38MAPK induced by AngⅡ in HUVEC.

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Available abstract

Aim To study the effect of angiotensin(1-7) on inhibiting the inflammation induced by angiotensinⅡ(AngⅡ).Methods Cultured human umbilical vein endothelial cells(HUVEC) were randomly dividied into different groups,then incubated in the presence of Ang(1-7),AngⅡ and the specific inhibitor of Ang(1-7),A-779,and so on.The phosphorylation of p38MAPK were determined by Western blot,and the mRNA for the mas receptor were determined by reverse transcriptional PCR. Results Ang(1-7) dose-dependently inhibited the phosphorylation of p38MAPK induced by AngⅡ in HUVECs.The expression of p38MAPK phosphorylation died down markedly at 1 000 nmol/L of Ang(1-7).Pre-treatment with A-779 for 10 min in HUVEC before Ang(1-7) and AngⅡ used,the expression of p38 MAPK phosphorylation was nonsignificantly changed. Conclusion Ang(1-7) effectively represses the phosphorylation of p38MAPK induced by AngⅡ in HUVEC.

Key concepts: Umbilical vein, Phosphorylation, p38 mitogen-activated protein kinases, Angiotensin II, Western blot, Kinase, Human umbilical vein endothelial cell, Renin–angiotensin system

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