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Published on: June 15, 2018
Overexpression of microRNA-99a Attenuates Cardiac Hypertrophy
Qiaoling Li1, Jun Xie1, Bingjian Wang2
1Department of Cardiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, Jiangsu, 210008, China.
Insights
MicroRNA-99a (miR-99a) negatively regulates cardiac hypertrophy by down-regulating the mammalian target of rapamycin (mTOR) pathway. This finding offers a potential new therapy for heart failure.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- MicroRNA Therapeutics
Background:
- Pathological cardiomyocyte hypertrophy is a key risk factor for heart failure.
- MicroRNAs are implicated in cardiac remodeling, but miR-99a's role is unclear.
Purpose of the Study:
- To investigate the role of miR-99a in cardiac hypertrophy.
- To determine if miR-99a influences the mammalian target of rapamycin (mTOR) signaling pathway.
Main Methods:
- Assessed miR-99a expression in cardiomyocytes and mice models of cardiac hypertrophy (isoprenaline/angiotensin-II and transverse aortic constriction).
- Evaluated miR-99a's effect on cardiac function and hypertrophy markers.
- Investigated the impact of miR-99a overexpression on mTOR signaling.
Main Results:
- miR-99a expression was reduced in hypertrophic conditions and correlated with cardiac dysfunction.
- Overexpression of miR-99a attenuated cardiac hypertrophy in both cellular and in vivo models.
- miR-99a exerted its protective effect by down-regulating mTOR expression.
Conclusions:
- miR-99a acts as a negative regulator of pathological cardiac hypertrophy.
- The miR-99a/mTOR signaling pathway presents a potential therapeutic target for heart failure.
- This study highlights miR-99a's significance in cardiac remodeling and function.
Abstract:
Pathological cardiomyocyte hypertrophy is associated with significantly increased risk of heart failure, one of the leading medical causes of mortality worldwide. MicroRNAs are known to be involved in pathological cardiac remodeling. However, whether miR-99a participates in the signaling cascade leading to cardiac hypertrophy is unknown. To evaluate the role of miR-99a in cardiac hypertrophy, we assessed the expression of miR-99a in hypertrophic cardiomyocytes induced by isoprenaline (ISO)/angiotensin-II (Ang II) and in mice model of cardiac hypertrophy induced by transverse aortic constriction (TAC). Expression of miR-99a was evaluated in these hypertrophic cells and hearts. We also found that miR-99a expression was highly correlated with cardiac function of mice with heart failure (8 weeks after TAC surgery). Overexpression of miR-99a attenuated cardiac hypertrophy in TAC mice and cellular hypertrophy in stimuli treated cardiomyocytes through down-regulation of expression of mammalian target of rapamycin (mTOR). These results indicate that miR-99a negatively regulates physiological hypertrophy through mTOR signaling pathway, which may provide a new therapeutic approach for pressure-overload heart failure.
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