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circRNA-miRNA Complex Participates in the Apoptosis of Myocardial Cells in Myocardial Ischemia/Reperfusion Injury
Yu Sun1, Yuanmei Zhang2, Zebing Ye1
1Department of Cardiac Intensive Care Unit, Cardiovascular Hospital, Guangdong Second Provincial General Hospital, Guangzhou, Guangdong, 510310, China.
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.
Insights
This study reveals that circ_Ddx60 protects against myocardial ischemia/reperfusion (I/R) injury by inhibiting cardiac cell apoptosis. It achieves this by regulating the miR-302a-3p/Bcl2a1a axis, offering new therapeutic insights.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- RNA Biology
Background:
- Myocardial ischemia/reperfusion (I/R) injury is a significant clinical challenge.
- Understanding the molecular mechanisms underlying I/R injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role and mechanism of circular RNA Ddx60 (circ_Ddx60) in a mouse model of myocardial I/R injury.
- To explore the regulatory pathway involving circ_Ddx60, miR-302a-3p, and Bcl2a1a in cardiac cells.
Main Methods:
- RNA sequencing and bioinformatics analysis to identify differentially expressed circRNAs and mRNAs.
- Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) for gene expression validation.
- Cellular assays to assess apoptosis and protein expression in HL-1 cells under hypoxia/reoxygenation (H/R).
Main Results:
- circ_Ddx60 was identified as differentially expressed in I/R injury and was upregulated in HL-1 cells under H/R conditions.
- Overexpression of circ_Ddx60 inhibited apoptosis and promoted Bcl2a1a expression in cardiac cells.
- circ_Ddx60 directly targets miR-302a-3p, and this interaction mediates the regulation of apoptosis and Bcl2a1a expression.
Conclusions:
- circ_Ddx60 plays a protective role in myocardial I/R injury by inhibiting apoptosis.
- The mechanism involves circ_Ddx60 regulating the miR-302a-3p/Bcl2a1a axis.
- This finding offers novel therapeutic targets for preventing myocardial I/R injury.
