CONTEXT:In animal models, estrogen inhibits atherogenesis by inhibiting many of the early steps of atherosclerotic plaque formation. However, the lack of cardioprotective effect by postmenopausal hormone replacement therapy and possible increase in cardiovascular events observed during the first year after the initiation of hormone replacement therapy may suggest that once the plaque is formed, estrogen may have additional effects that may counteract its beneficial outcomes. Indeed, the effect of estrogen on plaque stability has not been identified. OBJECTIVE:We hypothesized that 17beta-estradiol (E2) may cause increased apoptosis in human coronary artery endothelial cells (HCAECs). This effect would explain an adverse effect on plaque stability in vivo. INTERVENTION(S) AND MAIN OUTCOME MEASURE(S):The effect of E2 on apoptosis, cell proliferation, and expression of proapoptotic molecules Fas and Fas ligand (FasL) in cultured HCAECs was evaluated. RESULTS:HCAECs in culture treated with E2 showed an increase in DNA strand breaks and nuclear fragmentation indicative of apoptosis. E2 treatment also induced a significant concentration-dependent increase in Fas mRNA and protein expressions in HCAECs. Moreover, the expression of FasL mRNA and secretion of FasL protein by HCAECs were enhanced in response to E2 treatments. CONCLUSIONS:E2 increases the apoptosis in cultured HCAECs. Enhanced Fas and FasL expressions in response to E2 suggest that activation of the Fas/FasL pathway may be a mediator of the proapoptotic effects of E2 in these cells.

译文

背景:在动物模型中,雌激素通过抑制动脉粥样硬化斑块形成的许多早期步骤来抑制动脉粥样硬化。然而,绝经后激素替代疗法缺乏心脏保护作用,并且在开始激素替代疗法后的第一年观察到的心血管事件可能增加,这可能表明一旦形成斑块,雌激素可能会产生额外的作用,从而抵消其有益的结果。 。实际上,尚未确定雌激素对斑块稳定性的作用。
目的:我们假设17β-雌二醇(E2)可能导致人冠状动脉内皮细胞(HCAEC)凋亡增加。该作用将解释对体内斑块稳定性的不利影响。
干预和主要观察指标:评估了E2对培养的HCAEC中细胞凋亡,细胞增殖以及促凋亡分子Fas和FasL配体(FasL)表达的影响。
结果:用E2处理的培养物中的HCAECs显示DNA链断裂的增加和核碎裂指示凋亡。 E2处理还诱导了HCAECs Fas mRNA和蛋白表达的浓度依赖性显着增加。而且,响应于E2处理,HCAECs的FasL mRNA的表达和FasL蛋白的分泌得到增强。
结论:E2增加了培养的HCAECs的细胞凋亡。响应E2增强的Fas和FasL表达表明Fas / FasL途径的激活可能是这些细胞中E2促凋亡作用的介质。

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