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Published on: June 15, 2018
Overexpressing microRNA-203 alleviates myocardial infarction via interacting with long non-coding RNA MIAT and
Fan Wang1,2, Renliang Yu1,3, Shengnan Wen1
1Department of Cardiology, Shandong Provincial Qianfoshan Hospital Affiliated to Shandong University, 16766 Jingshi Rd., Jinan, 250014, Shandong Province, China.
Abstract:
Myocardial infarction (MI) is one of the leading causes of high mortality worldwide. Long non-coding RNA myocardial infarction associated transcript (MIAT) and mitochondrial coupling factor 6 (CF6) aggravate MI. This study aimed to elucidate whether miR-203 interacted with MIAT and CF6 in MI. Results revealed that MIAT and CF6 expressions were upregulated and that miR-203 was downregulated in mouse myocardial tissues after MI, as well as in hypoxic mouse cardiomyocytes. The overexpression of MIAT in mouse cardiomyocytes raised CF6 expression, whereas the knockdown of MIAT had the opposite effect. Mechanistically, the luciferase reporter and RNA pull-down assays corroborated the binding between miR-203 and CF6 3'UTR and between miR-203 and MIAT. The simultaneous overexpression of miR-203 and MIAT restored the reduction of CF6 caused by miR-203 overexpression alone, and the overexpression of miR-203 diminished the percentage of infarct area and the apoptosis of cardiomyocytes in vivo. Our findings corroborate that overexpressing miR-203 alleviates MI via interacting with MIAT and CF6.
Insights
This study reveals that overexpressing microRNA-203 (miR-203) alleviates myocardial infarction (MI) by interacting with myocardial infarction associated transcript (MIAT) and mitochondrial coupling factor 6 (CF6). This finding offers a potential therapeutic strategy for MI.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- RNA Biology
Background:
- Myocardial infarction (MI) is a major global cause of mortality.
- Long non-coding RNA MIAT and mitochondrial coupling factor 6 (CF6) are implicated in exacerbating MI.
- Understanding the molecular mechanisms underlying MI is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the interaction between miR-203, MIAT, and CF6 in the context of MI.
- To elucidate the role of miR-203 in regulating MIAT and CF6 expression.
- To determine the therapeutic potential of miR-203 in alleviating MI.
Main Methods:
- Analysis of MIAT, CF6, and miR-203 expression in mouse myocardial tissues and cardiomyocytes post-MI and hypoxia.
- In vitro experiments involving overexpression and knockdown of MIAT in cardiomyocytes.
- Luciferase reporter assays and RNA pull-down assays to confirm molecular interactions.
- In vivo studies to assess the effect of miR-203 overexpression on infarct size and cardiomyocyte apoptosis.
Main Results:
- MIAT and CF6 expression were upregulated, while miR-203 was downregulated in MI models.
- MIAT overexpression increased CF6 expression; MIAT knockdown decreased it.
- miR-203 directly binds to both MIAT and the 3'UTR of CF6.
- Overexpression of miR-203 reduced infarct area and cardiomyocyte apoptosis in vivo.
- Simultaneous overexpression of miR-203 and MIAT reversed the effects of miR-203 alone on CF6.
Conclusions:
- miR-203 plays a protective role in MI by targeting MIAT and CF6.
- The miR-203/MIAT/CF6 axis represents a novel regulatory pathway in MI pathogenesis.
- Overexpression of miR-203 demonstrates therapeutic potential for mitigating MI-induced damage.
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