2008Chinese Journal of HypertensionRequires access

Effect of Angiotensin(1-7) on the Expression of MCP-1 Induced by Oxidized LDL in Cultured Human Umbilical Vein Endothelial Cells

Lijun Wang

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Abstract

Objective To study the effect of Angiotensin(1—7)[Ang(1—7)] on the expression of monocyte chemotractive protein-1(MCP-1)induced by oxidized LDL(ox-LDL)in cultured human umbilical vein endothelial cells(HUVEC).Methods Original cultured HUVEC were incubated for 24 hours with different concentrations of Ang(1—7),ox-LDL and A-779 a specific inhibitor of Ang(1—7)alone or combination,respectively.The final concentrations of Ang(1—7)were 10,100 and 1000 nmol/L,and ox-LDL were 25,50 and 100 ng protein/L,re- spectively.The final concentration of A-779 [an Ang(1—7)receptor antagonist] was 100 nmol/L.MCP-1 anti- gen in the medium was determined by ELISA and its mRNA levels were determined by RT-PCR.Results Ox-LDL (on the range of 25—100 mg protein/L)dose-dependently increased MCP-1 release and up-regulated MCP-1 gene transcription(P0.05-0.01).Ang(1-7)did not affect the expression of MCP-1 at basal condition(P0.05) but inhibited the protein and gene expression of MCP-1 in a dose-dependent manner on the range of 10-1000 mmol/L(P 0.05-0.01).The effects of Ang(1—7)was prevented by A-779.Conclusion Angiotensin(1—7)effectively in- hibits the expression of monoeyte chemotractive protein-1 induced by oxidized LDL in HUVEC via its specific receptor.

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Objective To study the effect of Angiotensin(1—7)[Ang(1—7)] on the expression of monocyte chemotractive protein-1(MCP-1)induced by oxidized LDL(ox-LDL)in cultured human umbilical vein endothelial cells(HUVEC).Methods Original cultured HUVEC were incubated for 24 hours with different concentrations of Ang(1—7),ox-LDL and A-779 a specific inhibitor of Ang(1—7)alone or combination,respectively.The final concentrations of Ang(1—7)were 10,100 and 1000 nmol/L,and ox-LDL were 25,50 and 100 ng protein/L,re- spectively.The final concentration of A-779 [an Ang(1—7)receptor antagonist] was 100 nmol/L.MCP-1 anti- gen in the medium was determined by ELISA and its mRNA levels were determined by RT-PCR.Results Ox-LDL (on the range of 25—100 mg protein/L)dose-dependently increased MCP-1 release and up-regulated MCP-1 gene transcription(P0.05-0.01).Ang(1-7)did not affect the expression of MCP-1 at basal condition(P0.05) but inhibited the protein and gene expression of MCP-1 in a dose-dependent manner on the range of 10-1000 mmol/L(P 0.05-0.01).The effects of Ang(1—7)was prevented by A-779.Conclusion Angiotensin(1—7)effectively in- hibits the expression of monoeyte chemotractive protein-1 induced by oxidized LDL in HUVEC via its specific receptor.

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Available abstract

Objective To study the effect of Angiotensin(1—7)[Ang(1—7)] on the expression of monocyte chemotractive protein-1(MCP-1)induced by oxidized LDL(ox-LDL)in cultured human umbilical vein endothelial cells(HUVEC).Methods Original cultured HUVEC were incubated for 24 hours with different concentrations of Ang(1—7),ox-LDL and A-779 a specific inhibitor of Ang(1—7)alone or combination,respectively.The final concentrations of Ang(1—7)were 10,100 and 1000 nmol/L,and ox-LDL were 25,50 and 100 ng protein/L,re- spectively.The final concentration of A-779 [an Ang(1—7)receptor antagonist] was 100 nmol/L.MCP-1 anti- gen in the medium was determined by ELISA and its mRNA levels were determined by RT-PCR.Results Ox-LDL (on the range of 25—100 mg protein/L)dose-dependently increased MCP-1 release and up-regulated MCP-1 gene transcription(P0.05-0.01).Ang(1-7)did not affect the expression of MCP-1 at basal condition(P0.05) but inhibited the protein and gene expression of MCP-1 in a dose-dependent manner on the range of 10-1000 mmol/L(P 0.05-0.01).The effects of Ang(1—7)was prevented by A-779.Conclusion Angiotensin(1—7)effectively in- hibits the expression of monoeyte chemotractive protein-1 induced by oxidized LDL in HUVEC via its specific receptor.

Key concepts: Umbilical vein, Angiotensin II, Endocrinology, Internal medicine, Chemistry, Receptor, Human umbilical vein endothelial cell, Renin–angiotensin system

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