ITGB1 Suppresses Autophagy Through Inhibiting The mTORC2/AKT Signaling Pathway In H9C2 Cells.

Weiwei Zhou, Weizhe Liu, Dingyan Zhou, Aiying Li
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引用次数: 2

Abstract

Cardiomyocyte autophagy is closely related to myocardial infarction and hypertrophy. To study the molecular mechanism of autophagy is helpful for the prevention and treatment of these diseases. As a cell surface receptor, the function of ITGB1 gene in cardiomyocyte autophagy is not clear. The purpose of this research was to investigate the function and molecular mechanism of ITGB1 on autophagy. The autophagy-related marker proteins and signaling molecules were detected using western blot with knockdown and overexpression of ITGB1 in H9C2 cells. The results suggested that ITGB1 could inhibit autophagy and the mTORC2/Akt pathway molecules. To further investigate whether the effect of ITGB1 on autophagy might affect myocardial hypertrophy, we constructed AngII induced H9C2 cells and TAC induced rats models. The results showed that ITGB1 inhibited myocardial hypertrophy in both H9C2 cells and heart tissues of disease model. These data highlight the regulation mechanism on autophagy by ITGB1 and the potential usefulness of the gene as a potential target for preventing heart disease.
ITGB1通过抑制H9C2细胞mTORC2/AKT信号通路抑制自噬。
心肌细胞自噬与心肌梗死和心肌肥大密切相关。研究细胞自噬的分子机制有助于预防和治疗这些疾病。ITGB1基因作为细胞表面受体,在心肌细胞自噬中的作用尚不清楚。本研究旨在探讨ITGB1对细胞自噬的作用及其分子机制。western blot法检测H9C2细胞中ITGB1的自噬相关标记蛋白和信号分子表达。结果表明,ITGB1可以抑制自噬和mTORC2/Akt通路分子。为了进一步研究ITGB1对自噬的影响是否影响心肌肥大,我们构建了AngII诱导的H9C2细胞和TAC诱导的大鼠模型。结果显示,ITGB1对疾病模型H9C2细胞及心脏组织心肌肥厚均有抑制作用。这些数据强调了ITGB1对自噬的调控机制,以及该基因作为预防心脏病的潜在靶点的潜在用途。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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