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首页> 外文期刊>Journal of cellular physiology. >Bcl-2-associated athanogene 5 overexpression attenuates catecholamine-induced vascular endothelial cell apoptosis
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Bcl-2-associated athanogene 5 overexpression attenuates catecholamine-induced vascular endothelial cell apoptosis

机译:Bcl-2-associated athanogene 5超表达变弱catecholamine-induced血管内皮细胞凋亡

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摘要

Bcl-2 associated athanogene 5 (Bag5) is a novel endoplasmic reticulum (ER) regulator. However, its role in catecholamine-induced endothelial cells damage has not been fully understood. In our study, catecholamine was used to mimic hypertension-related endothelial cell damage. Then, western blots, enzyme-linked immunosorbent assay, immunofluorescence, quantitative polymerase chain reaction and pathway analysis were conducted to analyze the role of Bag5 in endothelial cell damage in response to catecholamine. Our results indicated that the endothelial cell viability was impaired by catecholamine. Interestingly, Bag5 overexpression significantly reversed endothelial cell viability. Mechanistically, Bag5 overexpression inhibited ER stress, attenuated oxidative stress and repressed inflammation in catecholamine-treated endothelial cells. These beneficial effects finally contributed to endothelial cell survival under catecholamine treatment. Pathway analysis demonstrated that Bag5 was under the control of the mitogen-activated protein kinase (MAPK)-extracellular-signal-regulated kinase (ERK) signaling pathway. Reactivation of the MAPK-ERK pathway could upregulate Bag5 expression and thus promote endothelial cell survival through inhibiting oxidative stress, ER stress, and inflammation. Altogether, our results illustrate that Bag5 overexpression sustains endothelial cell survival in response to catecholamine treatment. This finding identifies Bag5 downregulation and the inactivated MAPK-ERK pathway as potential mechanisms underlying catecholamine-induced endothelial cell damage.
机译:bcl - 2相关athanogene 5 (Bag5)是一部小说内质网(ER)监管机构。它在catecholamine-induced内皮中的作用细胞损伤没有被完全理解。我们的研究中,儿茶酚胺被用来模拟hypertension-related内皮细胞损伤。然后,西方的屁股,酶联免疫吸附试验、免疫荧光定量聚合酶链反应和路径分析进行分析的角色Bag5内皮细胞损伤的反应儿茶酚胺。内皮细胞的生存能力受到了损害儿茶酚胺。显著逆转内皮细胞生存能力。抑制ER压力,减少氧化应激和抑制炎症catecholamine-treated内皮细胞。最后导致有益的影响内皮细胞儿茶酚胺下生存治疗。Bag5的控制下增殖蛋白激酶(MAPK) -extracellular-signal-regulated激酶(ERK)信号通路。MAPK-ERK通路可能上调Bag5表达式从而促进内皮细胞的生存通过抑制氧化应激,ER应激,和炎症。说明Bag5过度支撑内皮细胞生存在回应儿茶酚胺治疗。和灭活MAPK-ERK差别Bag5对这些途径的潜在机制catecholamine-induced内皮细胞损伤。

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