The Influence of Angiotensin-(1-7) on the Secretion of E-selectin and Monocyte Chemotactic Protein-1 in Cultured Human Umbilical Vein Cells Induced by Angiotensin II
Na Zhang
Abstract
Na Zhang
Abstract
Aim To explore the influence of angiotensin-(1-7) [Ang-(1-7)] on the secretion of E-selectin(E-sel) and monocyte chemotactic protein-1(MCP-1) in cultured human umbilical vein cells induced by angiotensin Ⅱ(AngⅡ),and to clarify the antagonism of Ang-(1-7) on the inflammation induced by AngⅡ. Methods The cultured human umbilical vein endothelial cells(HUVECs) were randomly divided into control group,AngⅡ group,Ang-(1-7) group,Ang-(1-7)+AngⅡ group,and A-779+Ang-(1-7)+AngⅡ group.The expressions of E-sel and MCP-1 inprotein level and mRNA level were detected by enzyme linked immunosorbent assay(ELISA) and reverse transcription polymerase chain reaction(RT-PCR). Results ①Compared with the control group,100 nmol/L AngⅡ distinctly increased the protein of E-sel(25.39±1.97 μg/L) and MCP-1(238.71±5.51 ng/L) in HUVECs(P0.01),and significantly increased mRNA expression of E-sel and MCP-1 in HUVECs(P0.01).②Compared with the AngⅡ group,Ang-(1-7)(1 000 nmol/L) decreased the protein of E-sel(3.72±0.95 μg/L) and MCP-1(90.24±9.82 ng/L)(P0.01),and the mRNA expression of E-sel and MCP-1(P0.01).③10~10 000 nmol/L Ang-(1-7) attenuated the protein of E-sel in HUVECs induced by AngⅡ in a concentration dependent manner(21.15±1.31 μg/L,17.41±1.94 μg/L,12.71±1.84 μg/L and 9.46±1.40 μg/L)(P0.01),and also inhibited the protein of MCP-1 in HUVECs induced by AngⅡ in a concentration dependent manner(214.57±7.16 ng/L,196.83±8.20 ng/L,176.63±8.93 ng/L and 155.52±8.19 ng/L)(P0.01).④Compared with the AngⅡ group,10~10 000 nmol/L Ang-(1-7) inhibited the mRNA expression of E-sel and MCP-1 in HUVECs induced by AngⅡ in a dose dependent manner(P0.01).⑤The A-779 group had no significant deviation than the AngⅡ group(P0.05). Conclusions Ang-(1-7) inhibited the secretion of E-sel and MCP-1 in cultured HUVECs induced by AngⅡ in a concentration dependent matter.The inhibition effect of Ang-(1-7) may be through its specific receptor.
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Aim To explore the influence of angiotensin-(1-7) [Ang-(1-7)] on the secretion of E-selectin(E-sel) and monocyte chemotactic protein-1(MCP-1) in cultured human umbilical vein cells induced by angiotensin Ⅱ(AngⅡ),and to clarify the antagonism of Ang-(1-7) on the inflammation induced by AngⅡ. Methods The cultured human umbilical vein endothelial cells(HUVECs) were randomly divided into control group,AngⅡ group,Ang-(1-7) group,Ang-(1-7)+AngⅡ group,and A-779+Ang-(1-7)+AngⅡ group.The expressions of E-sel and MCP-1 inprotein level and mRNA level were detected by enzyme linked immunosorbent assay(ELISA) and reverse transcription polymerase chain reaction(RT-PCR). Results ①Compared with the control group,100 nmol/L AngⅡ distinctly increased the protein of E-sel(25.39±1.97 μg/L) and MCP-1(238.71±5.51 ng/L) in HUVECs(P0.01),and significantly increased mRNA expression of E-sel and MCP-1 in HUVECs(P0.01).②Compared with the AngⅡ group,Ang-(1-7)(1 000 nmol/L) decreased the protein of E-sel(3.72±0.95 μg/L) and MCP-1(90.24±9.82 ng/L)(P0.01),and the mRNA expression of E-sel and MCP-1(P0.01).③10~10 000 nmol/L Ang-(1-7) attenuated the protein of E-sel in HUVECs induced by AngⅡ in a concentration dependent manner(21.15±1.31 μg/L,17.41±1.94 μg/L,12.71±1.84 μg/L and 9.46±1.40 μg/L)(P0.01),and also inhibited the protein of MCP-1 in HUVECs induced by AngⅡ in a concentration dependent manner(214.57±7.16 ng/L,196.83±8.20 ng/L,176.63±8.93 ng/L and 155.52±8.19 ng/L)(P0.01).④Compared with the AngⅡ group,10~10 000 nmol/L Ang-(1-7) inhibited the mRNA expression of E-sel and MCP-1 in HUVECs induced by AngⅡ in a dose dependent manner(P0.01).⑤The A-779 group had no significant deviation than the AngⅡ group(P0.05). Conclusions Ang-(1-7) inhibited the secretion of E-sel and MCP-1 in cultured HUVECs induced by AngⅡ in a concentration dependent matter.The inhibition effect of Ang-(1-7) may be through its specific receptor.
Key concepts: Umbilical vein, Angiotensin II, Monocyte, Internal medicine, Endocrinology, Messenger RNA, Secretion, Chemotaxis