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Annexin A3 基因沉默通过激活急性心肌梗死大鼠的 PI3K/Akt 信号通路促进心肌细胞修复。

Annexin A3 gene silencing promotes myocardial cell repair through activation of the PI3K/Akt signaling pathway in rats with acute myocardial infarction.

机构信息

Department of Cardiology, Henan Provincial People's Hospital, Fuwai Central China Cardiovascular Hospital, Zhengzhou, China.

出版信息

J Cell Physiol. 2019 Jul;234(7):10535-10546. doi: 10.1002/jcp.27717. Epub 2018 Nov 19.

Abstract

Acute myocardial infarction (AMI), as a severe consequence of coronary atherosclerotic heart disease, always contributes to the loss of myocardial cells. Mounting evidence shows that annexin protects the myocardium from ischemic injury. In this study, we examine the inhibition of annexin A3 (ANXA3) on AMI through the phosphatidylinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. We selected rats to build an AMI model which was then assigned into different groups. The hemodynamic parameters after transfection were detected by using enzyme-linked immunosorbent assay. The effect of silencing of ANXA3 on inflammatory reaction and the PI3K/Akt signaling pathway was assessed. Rats transfected with ANXA3-short hairpin RNA had alleviated hemodynamics, inflammatory reaction, decreased infarct size, α-smooth muscle actin, Collagen I, and Collagen III as well as an increased vascular endothelial growth factor. Silencing ANAX3 would promote repair and healing of myocardial tissue by activation of the PI3K/Akt signaling pathway. Collectively, our study provides evidence that the downregulation of ANXA3 promotes the repair and healing of myocardial tissues by activating the PI3K/Akt signaling pathway.

摘要

急性心肌梗死(AMI)作为冠状动脉粥样硬化性心脏病的严重后果,总是导致心肌细胞的损失。越来越多的证据表明膜联蛋白 A3(ANXA3)通过磷脂酰肌醇 3-激酶/蛋白激酶 B(PI3K/Akt)信号通路保护心肌免受缺血性损伤。在这项研究中,我们通过 PI3K/Akt 信号通路研究了抑制膜联蛋白 A3(ANXA3)对 AMI 的作用。我们选择大鼠建立 AMI 模型,然后将其分为不同组。通过酶联免疫吸附试验检测转染后的血液动力学参数。评估沉默 ANXA3 对炎症反应和 PI3K/Akt 信号通路的影响。转染 ANXA3-short hairpin RNA 的大鼠缓解了血液动力学、炎症反应,减少了梗死面积、α-平滑肌肌动蛋白、胶原 I 和胶原 III,并增加了血管内皮生长因子。沉默 ANAX3 通过激活 PI3K/Akt 信号通路促进心肌组织的修复和愈合。总之,我们的研究提供了证据,表明下调 ANXA3 通过激活 PI3K/Akt 信号通路促进心肌组织的修复和愈合。

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