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心肌肌钙蛋白 I 自身抗体通过 PTEN 信号激活诱导心肌功能障碍。

Cardiac troponin I autoantibody induces myocardial dysfunction by PTEN signaling activation.

机构信息

Outpatient Department, Changcheng Hospital, Nanchang University, Nanchang, Jiangxi 330002, China; Department of Laboratory Medicine, Changhai Hospital, Second Military Medical University, Shanghai 200433, China.

Department of Laboratory Medicine, Changhai Hospital, Second Military Medical University, Shanghai 200433, China.

出版信息

EBioMedicine. 2019 Sep;47:329-340. doi: 10.1016/j.ebiom.2019.08.045. Epub 2019 Aug 29.

DOI:10.1016/j.ebiom.2019.08.045
PMID:31474552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6796505/
Abstract

BACKGROUND

The objective of the current study was to study the molecular mechanism(s) underlying cardiac troponin I autoantibody (cTnIAAb) binding to cardiomyocyte and resultant myocardial damage/dysfunction.

METHODS

cTnIAAb was purified from serum of 10 acute myocardial infarction (AMI) patients with left ventricular remodeling. Recombinant human cTnI was used to generate three mouse-derived monoclonal anti-cTnI antibodies (cTnImAb1, cTnImAb2, and cTnImAb3). The target proteins in cardiac myocyte membrane bound to cTnImAb and effect of cTnIAAb and cTnImAb on apoptosis and myocardial function were determined.

FINDINGS

We found that cTnIAAb/cTnImAb1 directly bound to the cardiomyocyte membraneα-Enolase (ENO1) and triggered cell apoptosis via increased expression of ENO1 and Bax, decreased expression of Bcl2, subsequently activating Caspase8, Caspase 3, phosphatase and tensin homolog (PTEN) while inhibiting Akt activity. This cTnIAAb-ENO1-PTEN-Akt signaling axis contributed to increased myocardial apoptosis, myocardial collagen deposition, and impaired systolic dysfunction.

INTERPRETATION

Results obtained in this study indicate that cTnIAAb is involved in the process of ventricular remodeling after myocardial injury. FUND: The National Natural Science Foundation of China (Grant#: 81260026).

摘要

背景

本研究旨在探讨心肌肌钙蛋白 I 自身抗体（cTnIAAb）与心肌细胞结合及导致心肌损伤/功能障碍的分子机制。

方法

从 10 例左心室重构的急性心肌梗死（AMI）患者的血清中纯化 cTnIAAb。使用重组人 cTnI 产生三种小鼠源性单克隆抗 cTnI 抗体（cTnImAb1、cTnImAb2 和 cTnImAb3）。确定与 cTnImAb 结合的心肌细胞膜上的靶蛋白，以及 cTnIAAb 和 cTnImAb 对细胞凋亡和心肌功能的影响。

结果

我们发现 cTnIAAb/cTnImAb1 直接与心肌细胞膜上的α-烯醇酶（ENO1）结合，通过增加 ENO1 和 Bax 的表达、降低 Bcl2 的表达，从而激活 Caspase8、Caspase 3、磷酸酶和张力蛋白同源物（PTEN），同时抑制 Akt 活性，触发细胞凋亡。cTnIAAb-ENO1-PTEN-Akt 信号轴导致心肌细胞凋亡增加、心肌胶原沉积和收缩功能障碍。

结论

本研究结果表明，cTnIAAb 参与心肌损伤后的心室重构过程。

基金

国家自然科学基金（项目编号：81260026）。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/89f284a08d88/gr16.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/98d47df2f8b1/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/4f2e7b71f625/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/ccab5c117e3a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/3baa417a7033/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/aca3e7bfde0c/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/bcd7fd87c8b9/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/aeda07f31de3/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/34ef6ef57776/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/1ea25d1e1bc5/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/e3eb0502feaf/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/ff739fd63c80/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/943393cbbf68/gr12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/a2f210898042/gr13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/548c71afa127/gr14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/a49a75c185d5/gr15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/6796505/89f284a08d88/gr16.jpg

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