Effects of angiotensin II and valsartan on expression of lectin-like oxidized low-density lipoprotein recepter-1 in cultured human umbilical vein endothlial cells
Hangping Yao
Abstract
Hangping Yao
Abstract
Objective To evaluate the effect of angiotensin II (AngII) and a specific type 1 angiotensin II receptor (AT1) antagonist, valsartan, on lectin like oxidized low density lipoprotein recpter 1 (LOX 1) mRNA and protein expression in cultured human umbilical vein endothlial cells(HUVECs) Methods Several groups of cultured HUVECs were incubated with AngII of 1×10 -5 ~1×10 -10 mol/L for 24 hours or with 1×10 -6 mol/L AngII for various times up to 48 hours In other groups of HUVECs, valsartan(1×10 -6 mol/L)was added to the culture medium half an hour before cells were incubated with 1×10 -6 mol/L AngII for 24 hours Then HUVECs LOX 1 protein expression was measured by endothlial cell enzyme linked immunosorbent assay(ELISA), and LOX 1 mRNA expression was detected by quantitative competitive reverse transcription polymerase chain reaction (RT PCR) Results AngII markedly induced the increase of HUVECs LOX 1 protein and mRNA expression The increase in LOX 1 expression was dependent on AngII concentration (1×10 -5 ~1×10 -10 mol/L) After treatment with 1×10 -6 mol/L AngII for 3 hours, HUVECs LOX 1 expression was elevated ( P 0 05) in HUVECs, reaching its maxium at 24~36 hours The effect of AngII were blocked by pretreatment of HUVECs with 1×10 -6 mol/L valsartan Conclusion AngII concentration dependently and time dependently upregulated Lox 1 expression in HUVECs AT1 blocker, valsartan, could block it These effects of AngII may contribute to the pathogenesis of atherosclerosis, and valsartan may produce anti atherosclerosis
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Objective To evaluate the effect of angiotensin II (AngII) and a specific type 1 angiotensin II receptor (AT1) antagonist, valsartan, on lectin like oxidized low density lipoprotein recpter 1 (LOX 1) mRNA and protein expression in cultured human umbilical vein endothlial cells(HUVECs) Methods Several groups of cultured HUVECs were incubated with AngII of 1×10 -5 ~1×10 -10 mol/L for 24 hours or with 1×10 -6 mol/L AngII for various times up to 48 hours In other groups of HUVECs, valsartan(1×10 -6 mol/L)was added to the culture medium half an hour before cells were incubated with 1×10 -6 mol/L AngII for 24 hours Then HUVECs LOX 1 protein expression was measured by endothlial cell enzyme linked immunosorbent assay(ELISA), and LOX 1 mRNA expression was detected by quantitative competitive reverse transcription polymerase chain reaction (RT PCR) Results AngII markedly induced the increase of HUVECs LOX 1 protein and mRNA expression The increase in LOX 1 expression was dependent on AngII concentration (1×10 -5 ~1×10 -10 mol/L) After treatment with 1×10 -6 mol/L AngII for 3 hours, HUVECs LOX 1 expression was elevated ( P 0 05) in HUVECs, reaching its maxium at 24~36 hours The effect of AngII were blocked by pretreatment of HUVECs with 1×10 -6 mol/L valsartan Conclusion AngII concentration dependently and time dependently upregulated Lox 1 expression in HUVECs AT1 blocker, valsartan, could block it These effects of AngII may contribute to the pathogenesis of atherosclerosis, and valsartan may produce anti atherosclerosis
Key concepts: Valsartan, Angiotensin II, Umbilical vein, Angiotensin II receptor type 1, Chemistry, Messenger RNA, Renin–angiotensin system, Receptor