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首页> 外文期刊>American Journal of Physiology >Rapid estrogen receptor-a signaling mediated by ERK activation regulates vascular tone in male and ovary-intact female mice
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Rapid estrogen receptor-a signaling mediated by ERK activation regulates vascular tone in male and ovary-intact female mice

机译：快速雌激素受体 - 通过ERK活化介导的信号传导调节血管中的血管基调，血管完整的雌性小鼠

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Estrogen has been shown to affect vascular reactivity. Here, we assessed the estrogen receptor-a (ERa) dependency of estrogenic effects on vasorelaxation via a rapid non-genomic pathway in both male and ovary-intact female mice. We compared the effect of a primary estrogen, 17β-estradiol (E_2) or 4,4',4"-(4-propyl-[lH]pyrazole-l,3,5-triyl)tris-phenol (PPT; selective ERa agonist). We found that E_2 and PPT induced greater aortic relaxation in female mice than in male mice, indicating ERa mediation, which was further validated by using ERa antagonism. Treatment with 1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinyle-thoxy)phenol]-lH-pyrazole dihydrochloride (MPP dihydrochloride; ERa antagonist) attenuated PPT-mediated vessel relaxation in both sexes. ERa-mediated vessel relaxation was further validated by the absence of significant PPT-mediated relaxation in aortas isolated from ERa knockout mice. Treatment with a specific ERK inhibitor, PD-98059, reduced E_2-induced vessel relaxation in both sexes but to a lesser extent in female mice. Furthermore, PD-98059 prevented PPT-induced vessel relaxation in both sexes. Both E_2 and PPT treatment activated ERK as early as 5-10 min, which was attenuated by PD-98059 in aortic tissue, cultured primary vascular smooth muscle cells (VSMCs), and endothelial cells (ECs). Aortic rings denuded of endothelium showed no differences in vessel relaxation after E_2 or PPT treatment, implicating a role of ECs in the observed sex differences. Here, our results are unique to show estrogen-stimulated rapid ERa signaling mediated by ERK activation in aortic tissue, as well as VSMCs and ECs in vitro, in regulating vascular function by using side-by-side comparisons in male and ovary-intact female mice in response to E_2 or PPT.
机译：已显示雌激素影响血管反应性。在这里，我们评估了雌激素受体-A（ERA）雌激素作用对雌激素的依赖性通过雄性和卵巢完整的雌性小鼠的快速非基因组途径对血管结节。我们比较了初级雌激素，17β - 雌二醇（E_2）或4,4'，4,4“ - （4-丙基-1H]吡唑-1,3,5-三酯）三苯酚（PPT;选择性时代的效果激动剂）。我们发现E_2和PPT在雌性小鼠中诱导了比雄性小鼠更大的主动脉弛豫，表明ERA调解，通过使用时代拮抗作用进一步验证。用1,3-双（4-羟基苯基）-4-甲基处理-5- [4-（2-哌啶物 - 丁香）苯酚] -LH-吡唑二盐酸盐（MPP二盐酸盐;时代拮抗剂）减弱介导的两种性别的血管松弛。通过显着的不存在进一步验证了ERA介导的血管弛豫PPT介导的放松在从时代敲除小鼠隔离的主动脉。用特定ERK抑制剂的处理，PD-98059，在两性的血管松弛降低，但在雌性小鼠的程度上较小。此外，PD-98059预防PPT诱导两性的船只放松。E_2和PPT治疗早5-10分钟激活ERK，它由PD-98059 I衰减n主动脉组织，培养的原发性血管平滑肌细胞（VSMC）和内皮细胞（ECS）。内皮剥去的主动脉戒指在E_2或PPT处理后血管松弛没有差异，这意味着ECS在观察到的性差异中的作用。在这里，我们的结果是在体外组织中的ERK激活中介导的ERK激活介导的雌激素刺激的快速时代信号是独一无二的，并且在体外，通过使用雄性和卵巢完整的女性并行比较来调节血管功能响应E_2或PPT的小鼠。

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