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. 2016;39(4):1503-11.
doi: 10.1159/000447853. Epub 2016 Sep 12.

Cardiac-Specific Overexpression of miR-222 Induces Heart Failure and Inhibits Autophagy in Mice

Ming Su  1 , Zhiguo Chen, Changxin Wang, Lei Song, Yubao Zou, Lianfeng Zhang, Rutai Hui, Jizheng Wang
Affiliations
Free article

Cardiac-Specific Overexpression of miR-222 Induces Heart Failure and Inhibits Autophagy in Mice

Ming Su et al. Cell Physiol Biochem. 2016.
Free article

Abstract

Background: MicroRNAs play a crucial role in the regulation of pathological cardiac remodeling and heart failure. Previously, we found that overexpression of miR-221 induces heart failure in mice. The miR-222 and miR-221 share the same gene cluster, however, the role of miR-222 in the regulation of cardiac function remained ill-defined.

Methods and results: Transgenic mice with cardiac-specific expression of miR-222 (Tg-miR-222) mice were generated. The Tg-miR-222 mice developed significantly enlarged hearts at 4 weeks of age. Transthoracic echocardiograph data indicated that the hearts of Tg-miR-222 mice exhibited an increased left ventricular end-diastolic internal diameter and decreased fractional shortening. We observed that the LC3-II in Tg-miR-222 mice was decreased accompanied with the upregulation of p62, indicating the autophagy inhibition in the hearts of Tg-miR-222 mice. The mTOR pathway, a negative regulator of autophagy, was activated in the hearts of Tg-miR-222 mice. The expression of p27 was downregulated by miR-222 overexpression.

Conclusion: Our data indicate that miR-222 overexpression induces heart failure in mice. The downregulation of p27 and the activation of mTOR pathway may be involved in miR-222-induced heart failure and autophagy inhibition. Thus, targeting miR-222 expression may be a therapeutic strategy against pathological cardiac remodeling.

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