Myosin 1b参与缺氧/复氧诱导的H9c2细胞凋亡和自噬的调节。

IF 2.6 4区 医学 Q3 CELL BIOLOGY
Analytical Cellular Pathology Pub Date : 2022-11-22 eCollection Date: 2022-01-01 DOI:10.1155/2022/5187304
Jing Xu, Jin Huang, Xiaojie He, Mingshuang Hu, Shan Su, Ping Liu
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引用次数: 2

摘要

心肌缺血再灌注(I/R)损伤严重威胁着缺血性心脏病患者的健康和生命。本研究探讨了肌球蛋白1b (myo1b)对缺氧/再氧化- (H/R-)刺激的心肌细胞H9c2细胞凋亡和自噬的潜在影响。H/R刺激后,采用qRT-PCR检测H9c2细胞myo1b mRNA表达水平。将Myo1b过表达质粒(OE-myo1b)和靶向Myo1b的小干扰RNA (siRNA) (si-myo1b)转染H9c2细胞,改变H9c2细胞中Myo1b的表达。H/R刺激和/或转染OE-myo1b(或si-myo1b)后,分别检测H9c2细胞凋亡、增殖和自噬。我们发现H/R刺激降低了H9c2细胞myo1b mRNA水平,导致H9c2细胞凋亡、增殖抑制和自噬。myo1b的过表达逆转了H/ r导致的H9c2细胞凋亡、增殖抑制和自噬。myo1b沉默则相反,促进H9c2细胞凋亡,降低细胞增殖,加速细胞自噬。综上所述,Myo1b参与了H/R刺激的心肌细胞凋亡和自噬的调节,可能是预防和治疗I/R损伤的潜在内源性靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Myosin 1b Participated in the Modulation of Hypoxia/Reoxygenation-Caused H9c2 Cell Apoptosis and Autophagy.

Myosin 1b Participated in the Modulation of Hypoxia/Reoxygenation-Caused H9c2 Cell Apoptosis and Autophagy.

Myosin 1b Participated in the Modulation of Hypoxia/Reoxygenation-Caused H9c2 Cell Apoptosis and Autophagy.

Myosin 1b Participated in the Modulation of Hypoxia/Reoxygenation-Caused H9c2 Cell Apoptosis and Autophagy.

Myocardial ischemia/reperfusion (I/R) injury seriously threats the health and life of patients with ischemia heart disease. Herein, we probed the potential influence of myosin 1b (myo1b) on hypoxia/reoxygenation- (H/R-) stimulated cardiomyocyte H9c2 cell apoptosis and autophagy. After H/R stimulation, the myo1b mRNA level in H9c2 cells was tested via qRT-PCR. Myo1b overexpression plasmid (OE-myo1b) and small interfering RNA (siRNA) targeting myo1b (si-myo1b) were transfected into H9c2 cells to alter myo1b expression in H9c2 cells. Following H/R stimulation and/or OE-myo1b (or si-myo1b) transfection, H9c2 cell apoptosis, proliferation, and autophagy were detected, respectively. We found that H/R stimulation reduced the mRNA level of myo1b in H9c2 cells and resulted in H9c2 cell apoptosis, proliferation inhibition, and autophagy. Overexpression of myo1b reversed the H/R-resulted H9c2 cell apoptosis, proliferation inhibition, and autophagy. Silence of myo1b had opposite effects, which promoted H9c2 cell apoptosis, reduced cell proliferation, and accelerated cell autophagy. Taken together, Myo1b took part in the modulation of H/R-stimulated cardiomyocyte apoptosis and autophagy, which might be serve as a potential endogenous target for prevention and therapy of I/R injury.

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来源期刊
Analytical Cellular Pathology
Analytical Cellular Pathology ONCOLOGY-CELL BIOLOGY
CiteScore
4.90
自引率
3.10%
发文量
70
审稿时长
16 weeks
期刊介绍: Analytical Cellular Pathology is a peer-reviewed, Open Access journal that provides a forum for scientists, medical practitioners and pathologists working in the area of cellular pathology. The journal publishes original research articles, review articles, and clinical studies related to cytology, carcinogenesis, cell receptors, biomarkers, diagnostic pathology, immunopathology, and hematology.
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