• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >17beta-estradiol inhibits cyclic strain-induced endothelin-1 gene expression within vascular endothelial cells.
【24h】

17beta-estradiol inhibits cyclic strain-induced endothelin-1 gene expression within vascular endothelial cells.

机译：17β-雌二醇抑制循环应变诱导的血管内皮细胞内内皮素-1基因的表达。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

It has been well documented previously that 17beta-estradiol (E2) exerts a protective effect on cardiovascular tissue. The possible role of E2 in the regulation of endothelin (ET)-1 production has been previously reported, although the complex mechanisms by which E2 inhibits ET-1 expression are not completely understood. The aims of this study were to examine whether E2 was able to alter strain-induced ET-1 gene expression and also to identify the putative underlying signaling pathways that exist within endothelial cells. For cultured endothelial cells, E2 (1-100 nM), but not 17alpha-estradiol, inhibited the level of strain-induced ET-1 gene expression and also peptide secretion. This inhibitory effect elicited by E2 was able to be prevented by the coincubation of endothelial cells with the estrogen receptor antagonist ICI-182,780 (1 microM). E2 also inhibited strain-enhanced NADPH oxidase activity and intracellular reactive oxygen species (ROS) generation as measured by the redox-sensitive fluorescentdye 2',7'-dichlorofluorescin diacetate and the level of extracellular signal-regulated kinase (ERK) phosphorylation. Furthermore, the presence of E2 and antioxidants such as N-acetylcysteine and diphenylene iodonium were able to elicit a decrease in the level of strain-induced ET-1 secretion, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1 binding activity. In summary, we demonstrated, for the first time, that E2 inhibits strain-induced ET-1 gene expression, partially by interfering with the ERK pathway via the attenuation of strain-induced ROS generation. Thus this study delivers important new insight regarding the molecular pathways that may contribute to the proposed beneficial effects of estrogen on the cardiovascular system.
机译：以前已经有充分的文献证明17β-雌二醇（E2）对心血管组织具有保护作用。尽管尚不完全了解E2抑制ET-1表达的复杂机制，但E2在调节内皮素（ET）-1产生中的可能作用已有报道。这项研究的目的是检查E2是否能够改变菌株诱导的ET-1基因表达，并确定内皮细胞内存在的潜在信号通路。对于培养的内皮细胞，E2（1-100 nM），而不是17α-雌二醇，抑制菌株诱导的ET-1基因表达水平以及肽分泌。 E2引起的这种抑制作用可以通过将内皮细胞与雌激素受体拮抗剂ICI-182,780（1 microM）共孵育来预防。 E2还抑制了菌株增强的NADPH氧化酶活性和细胞内活性氧（ROS）的生成，这是通过氧化还原敏感的荧光染料2'，7'-二氯荧光素二乙酸盐和细胞外信号调节激酶（ERK）磷酸化的水平来衡量的。此外，E2和抗氧化剂（例如N-乙酰半胱氨酸和二亚苯基碘鎓）的存在能够引起菌株诱导的ET-1分泌，ET-1启动子活性，ET-1 mRNA，ERK磷酸化和激活剂水平降低蛋白1结合活性。总而言之，我们首次证明了E2抑制了菌株诱导的ET-1基因表达，部分是通过减弱菌株诱导的ROS生成来干扰ERK途径。因此，本研究提供了有关可能有助于雌激素对心血管系统有益作用的分子途径的重要新见解。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号