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POSTN 及其可变剪接对急性心肌梗死中心肌细胞凋亡的影响及机制：体外研究。

The Effect and Mechanism of POSTN and Its Alternative Splicing on the Apoptosis of Myocardial Cells in Acute Myocardial Infarction: A Study in Vitro.

机构信息

Department of Respiratory Medicine, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.

The Second Department of Coronary Heart Disease, the First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.

出版信息

Cell Biochem Biophys. 2023 Sep;81(3):481-491. doi: 10.1007/s12013-023-01157-w. Epub 2023 Aug 12.

DOI:10.1007/s12013-023-01157-w
PMID:37572219
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10465634/
Abstract

Our study aimed to investigate key molecular targets in the pathogenesis of AMI, and provide new strategy for the treatment. In this work, the myocardial ischemia and hypoxia model was constructed by using HL-1 mouse cardiomyocytes. The over-expressing POSTN wild-type, mutant and negative control lentiviruses (GV492-POSTNWT,GV492-POSTN-MUT, GV492-NC) was conducted and transfected. Cardiomyocytes were examined for cell proliferation and apoptosis to explore the effects of POSTN and its alternative splicing. The endoplasmic reticulum stess-related apoptosis proteins were selected and detected. We found that POSTN could promote the proliferation of normal and hypoxic cardiomyocytes and inhibit their apoptosis. The mechanism by which POSTN inhibited cardiomyocyte apoptosis may be through inhibiting the GRP78-eIF2α-ATF4-CHOP pathway of endoplasmic reticulum stress. Alternative splicing of POSTN could inhibit the apoptosis of ischemic and hypoxic cardiomyocytes, and its mechanism needs to be confirmed by further studies. We drawed the conclusion that POSTN might be a potential therapeutic target for AMI.

摘要

我们的研究旨在探讨 AMI 发病机制中的关键分子靶点，并为其治疗提供新策略。本研究采用 HL-1 小鼠心肌细胞构建心肌缺血缺氧模型，过表达 POSTN 野生型、突变型和阴性对照慢病毒（GV492-POSTNWT、GV492-POSTN-MUT、GV492-NC）并转染。检测细胞增殖和凋亡，探讨 POSTN 及其选择性剪接的作用。选择并检测内质网应激相关凋亡蛋白。我们发现 POSTN 可促进正常和缺氧心肌细胞的增殖，抑制其凋亡。POSTN 抑制心肌细胞凋亡的机制可能是通过抑制内质网应激的 GRP78-eIF2α-ATF4-CHOP 通路。POSTN 的选择性剪接可以抑制缺血缺氧心肌细胞的凋亡，其机制还需要进一步研究证实。我们得出结论，POSTN 可能是 AMI 的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/c103e52018c0/12013_2023_1157_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/3d6d617e6e50/12013_2023_1157_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/3f972a6a2fce/12013_2023_1157_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/a8c8f1aa81cc/12013_2023_1157_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/af7d24dd8387/12013_2023_1157_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/c103e52018c0/12013_2023_1157_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/3d6d617e6e50/12013_2023_1157_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/3f972a6a2fce/12013_2023_1157_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/a8c8f1aa81cc/12013_2023_1157_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/af7d24dd8387/12013_2023_1157_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bc1/10465634/c103e52018c0/12013_2023_1157_Fig5_HTML.jpg

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