首页> 美国卫生研究院文献>Oxidative Medicine and Cellular Longevity >MicroRNA-33-3p Regulates Vein Endothelial Cell Apoptosis in Selenium-Deficient Broilers by Targeting E4F1
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MicroRNA-33-3p Regulates Vein Endothelial Cell Apoptosis in Selenium-Deficient Broilers by Targeting E4F1

机译:MicroRNA-33-3p通过靶向E4F1调节缺硒肉鸡的静脉内皮细胞凋亡

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摘要

Selenium (Se) is a type of nutrient element. The tissues of organisms can have pathological damage, including apoptosis, due to Se deficiency. Apoptosis is an important cell process and plays a key role in vascular disease and Se-deficient symptoms. In this study, the Se-deficient broiler model was duplicated, miR-33-3p in the vein was overexpressed in response to Se-deficiency, and miR-33-3p target gene E4F transcription factor 1 (E4F1) expression was also confirmed. We utilized ectopic miR-33-3p expression to validate its function for apoptosis. The results showed that miR-33-3p-targeted E4F1 are involved in the glucose-regulated protein 78- (GRP78-) induced endoplasmic reticulum stress (ERS) apoptosis pathway. We presumed that Se deficiency might trigger apoptosis via downregulating miR-33-3p. Interestingly, the miR-33-3p inhibitor and VER-155008 (GRP78 inhibitor) partly hindered the apoptosis caused by Se deficiency. Thus, the above information provides a new avenue toward understanding the mechanism of Se deficiency and reveals a novel apoptotic injury regulation model in vascular disease.
机译:硒(Se)是一种营养元素。由于硒缺乏,生物组织可能具有病理损伤,包括凋亡。凋亡是重要的细胞过程,在血管疾病和硒缺乏症状中起关键作用。在这项研究中,复制了Se缺乏型肉鸡模型,响应Se缺乏症,miR-33-3p在静脉中过表达,并且还证实了miR-33-3p目标基因E4F转录因子1(E4F1)的表达。我们利用异位miR-33-3p表达来验证其凋亡功能。结果表明,靶向miR-33-3p的E4F1参与了葡萄糖调节蛋白78-(GRP78-)诱导的内质网应激(ERS)凋亡途径。我们推测硒缺乏可能通过下调miR-33-3p触发凋亡。有趣的是,miR-33-3p抑制剂和VER-155008(GRP78抑制剂)部分阻止了Se缺乏引起的细胞凋亡。因此,以上信息为了解硒缺乏的机理提供了新途径,并揭示了血管疾病中新的细胞凋亡调控模型。

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