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LncRNA Gm4419 Regulates Myocardial Ischemia/Reperfusion Injury Through Targeting the miR-682/TRAF3 Axis
Guixiang Zhao1, Juledezi Hailati2, Xiaoyun Ma2
1Department of Cardiology, the Sixth Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang Uygur Autonomous Region, China.
Abstract:
Myocardial cell death during acute myocardial infarction occurs because of acute ischemia, persistent ischemia, reperfusion-associated injury, and the inflammatory infiltrate as a response to cell necrosis. In the present study, quantitative real-time PCR showed that lncRNA Gm4419 was highly upregulated in ischemia/reperfusion myocardial tissues and hypoxia/reoxygenation H9C2 cells, whereas miR-682 was downregulated. Knocking down Gm4419 with sh-Gm4419 resulted in the rescue of myocardial infarction and apoptosis induced by ischemia/reperfusion or hypoxia/reoxygenation. Our study further demonstrated that Gm4419 may bind with miR-682 directly. Moreover, in vitro experiments further demonstrated that miR-682 could bind to tumor necrosis factor receptor-associated factor 3 (TRAF3) directly. Most importantly, TRAF3 overexpression could counteract the effect of sh-Gm4419. Taken together, our study indicated that Gm4419 may target miR-682 via sponging to increase TRAF3 expression, thereby contributing to myocardial I/R injury. Therefore, the Gm4419/miR-682/TRAF3 axis may be an important regulatory mechanism in myocardial ischemia/reperfusion injury.
Insights
Long non-coding RNA Gm4419 exacerbates myocardial ischemia/reperfusion injury by sponging miR-682, leading to increased tumor necrosis factor receptor-associated factor 3 (TRAF3) expression. Targeting this Gm4419/miR-682/TRAF3 axis may offer a novel therapeutic strategy for heart attack.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Mechanisms of Heart Disease
Background:
- Myocardial infarction involves cell death from ischemia, reperfusion injury, and inflammation.
- Understanding molecular regulators of myocardial ischemia/reperfusion (I/R) injury is crucial for developing treatments.
Purpose of the Study:
- To investigate the role of long non-coding RNA Gm4419 in myocardial I/R injury.
- To elucidate the molecular mechanism involving Gm4419, miR-682, and tumor necrosis factor receptor-associated factor 3 (TRAF3) in cardiac injury.
Main Methods:
- Quantitative real-time PCR to assess gene expression in I/R tissues and cells.
- In vitro experiments using cell models (H9C2 cells) under hypoxia/reoxygenation.
- Genetic manipulation (sh-Gm4419 knockdown, TRAF3 overexpression) and molecular binding assays.
Main Results:
- Gm4419 was upregulated, while miR-682 was downregulated in myocardial I/R and hypoxia/reoxygenation models.
- Knockdown of Gm4419 protected against myocardial infarction and apoptosis.
- Gm4419 directly sponges miR-682, and miR-682 targets TRAF3; TRAF3 overexpression reversed the protective effects of Gm4419 knockdown.
Conclusions:
- The Gm4419/miR-682/TRAF3 axis promotes myocardial I/R injury by Gm4419 sponging miR-682 to upregulate TRAF3.
- This regulatory axis represents a potential therapeutic target for mitigating cardiac damage during heart attacks.
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