circRNA-miRNA Complex Participates in the Apoptosis of Myocardial Cells in Myocardial Ischemia/Reperfusion Injury.

IF 2 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Discovery medicine Pub Date : 2022-01-01
Yu Sun, Yuanmei Zhang, Zebing Ye, Yan Wang, Yu Lao, Juhong Zhang, Ming Fang, Jie He, Hao Yin, Wen Yan, Wen Jin
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引用次数: 0

Abstract

Myocardial ischemia/reperfusion (I/R) injury is a common condition. This study aimed to investigate the potential mechanisms of circ_Ddx60 in the mouse model of I/R injury. Cardiac tissues were used to extract RNA for subsequent RNA sequencing analysis. Bioinformatic analysis was performed and circ_Ddx60 and Bcl2a1a (B cell leukemia/lymphoma 2 related protein A1a) were selected for further validation. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was used to detect the gene expression level. The effect of circ_Ddx60 on cardiac cell apoptosis was examined. The function of miR-302a-3p in cell apoptosis was further explored in circ_Ddx60-overexpressed HL-1 cells under hypoxia/reoxygenation (H/R) treatment. We have revealed a number of differentially expressed circRNAs and mRNAs between the I/R group and sham groups, with circ_Ddx60 being among them. Treatment of HL-1 cells with hypoxia/reoxygenation (H/R) led to an overexpression of circ_Ddx60, which then inhibited apoptosis and promoted the Bcl2a1a expression. Furthermore, circ_Ddx60 directly binds with miR-302a-3p, which could reverse the effect of circ_Ddx60 overexpression on cellular apoptosis and Bcl2a1a expression. Our study revealed that circ_Ddx60 inhibits apoptosis in myocardial cells by regulating the miR-302a-3p/Bcl2a1a axis, which provides novel insights into the prevention of myocardial I/R injury.

circRNA-miRNA复合物参与心肌缺血/再灌注损伤时心肌细胞的凋亡
心肌缺血/再灌注(I/R)损伤是一种常见的疾病。本研究旨在探讨circ_Ddx60在I/R损伤小鼠模型中的潜在机制。心脏组织提取RNA用于后续的RNA测序分析。进行生物信息学分析,选择circ_Ddx60和Bcl2a1a (B细胞白血病/淋巴瘤2相关蛋白A1a)进行进一步验证。采用定量逆转录聚合酶链反应(qRT-PCR)检测基因表达水平。观察circ_Ddx60对心肌细胞凋亡的影响。在缺氧/再氧化(H/R)处理下circ_ddx60过表达的HL-1细胞中进一步探讨miR-302a-3p在细胞凋亡中的作用。我们已经揭示了I/R组和sham组之间一些差异表达的circrna和mrna, circ_Ddx60就是其中之一。缺氧/再氧化(H/R)处理HL-1细胞导致circ_Ddx60过表达,从而抑制细胞凋亡,促进Bcl2a1a表达。此外,circ_Ddx60直接与miR-302a-3p结合,可以逆转circ_Ddx60过表达对细胞凋亡和Bcl2a1a表达的影响。我们的研究发现circ_Ddx60通过调节miR-302a-3p/Bcl2a1a轴抑制心肌细胞凋亡,这为心肌I/R损伤的预防提供了新的见解。
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来源期刊
Discovery medicine
Discovery medicine MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
5.40
自引率
0.00%
发文量
80
审稿时长
6-12 weeks
期刊介绍: Discovery Medicine publishes novel, provocative ideas and research findings that challenge conventional notions about disease mechanisms, diagnosis, treatment, or any of the life sciences subjects. It publishes cutting-edge, reliable, and authoritative information in all branches of life sciences but primarily in the following areas: Novel therapies and diagnostics (approved or experimental); innovative ideas, research technologies, and translational research that will give rise to the next generation of new drugs and therapies; breakthrough understanding of mechanism of disease, biology, and physiology; and commercialization of biomedical discoveries pertaining to the development of new drugs, therapies, medical devices, and research technology.
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