2009Zhongguo bingli shengli zazhiRequires access

Effect of caveolin-1 and ERK1/2 on 17β-estradiol-induced inhibition of VSMC proliferation

Wang Ting-huai

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Abstract

AIM:To investigate the effect of caveolin-1 and phosphorylation of ERK1/2 on 17β-estradiol (E2) induced inhibition of vascular smooth muscle cells (VSMCs). METHODS:The proliferation in cultured VSMCs was determined by using [3H]-thymidine incorporation. The expressions of caveolin-1,MKP-1 and ERK1/2 phosphorylation were measured by Western blotting. The expression of caveolin-1 mRNA was measured by RT-PCR. RESULTS:Exposed to fetal calf serum (FCS) for 24 h,the increase in proliferation of VSMCs was detected by [3H]-thymidine incorporation. Pretreatment with various concentrations of E2 for 24 h inhibited VSMC proliferation induced by FCS. The results of Western blotting and RT-PCR showed that pretreated with 17β-estradiol for 24 h reserved the decrease in caveolin-1 induced by FCS. Western blotting results further proved that the expression of MKP-1 was significantly increased and the expression of ERK1/2 phosphorylation was decreased after incubated with 17β-estradiol. CONCLUSION:17β-estradiol increases caveolin-1 and MKP-1 expressions,and decreases ERK1/2 phosphorylation,leading to the inhibition of VSMC proliferation.

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AIM:To investigate the effect of caveolin-1 and phosphorylation of ERK1/2 on 17β-estradiol (E2) induced inhibition of vascular smooth muscle cells (VSMCs). METHODS:The proliferation in cultured VSMCs was determined by using [3H]-thymidine incorporation. The expressions of caveolin-1,MKP-1 and ERK1/2 phosphorylation were measured by Western blotting. The expression of caveolin-1 mRNA was measured by RT-PCR. RESULTS:Exposed to fetal calf serum (FCS) for 24 h,the increase in proliferation of VSMCs was detected by [3H]-thymidine incorporation. Pretreatment with various concentrations of E2 for 24 h inhibited VSMC proliferation induced by FCS. The results of Western blotting and RT-PCR showed that pretreated with 17β-estradiol for 24 h reserved the decrease in caveolin-1 induced by FCS. Western blotting results further proved that the expression of MKP-1 was significantly increased and the expression of ERK1/2 phosphorylation was decreased after incubated with 17β-estradiol. CONCLUSION:17β-estradiol increases caveolin-1 and MKP-1 expressions,and decreases ERK1/2 phosphorylation,leading to the inhibition of VSMC proliferation.

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Available abstract

AIM:To investigate the effect of caveolin-1 and phosphorylation of ERK1/2 on 17β-estradiol (E2) induced inhibition of vascular smooth muscle cells (VSMCs). METHODS:The proliferation in cultured VSMCs was determined by using [3H]-thymidine incorporation. The expressions of caveolin-1,MKP-1 and ERK1/2 phosphorylation were measured by Western blotting. The expression of caveolin-1 mRNA was measured by RT-PCR. RESULTS:Exposed to fetal calf serum (FCS) for 24 h,the increase in proliferation of VSMCs was detected by [3H]-thymidine incorporation. Pretreatment with various concentrations of E2 for 24 h inhibited VSMC proliferation induced by FCS. The results of Western blotting and RT-PCR showed that pretreated with 17β-estradiol for 24 h reserved the decrease in caveolin-1 induced by FCS. Western blotting results further proved that the expression of MKP-1 was significantly increased and the expression of ERK1/2 phosphorylation was decreased after incubated with 17β-estradiol. CONCLUSION:17β-estradiol increases caveolin-1 and MKP-1 expressions,and decreases ERK1/2 phosphorylation,leading to the inhibition of VSMC proliferation.

Key concepts: Blot, Vascular smooth muscle, Phosphorylation, Caveolin 1, Cell growth, Thymidine, Biology, Internal medicine

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