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HMGA1 Is a New Target of miR-195 Involving Isoprenaline-Induced Cardiomyocyte Hypertrophy

Xiang-Yu You#, Jiong-Hua Huang#, Bin Liu, Shao-Jun Liu, Yun Zhong, and Shi-Ming Liu*

Cardiovascular Department, Second Hospital Affiliated to Guangzhou Medical University, Guangzhou Institute of Cardiovascular Disease, 250 Chang-gang East Road, Guangzhou 510260, PR China; fax: +86 (20) 34153566; E-mail: gzliushiming@126.com; limnamil@163.com; huangjionghua2011@126.com; xmhoolv@163.com; shaojunliu@yahoo.com; dr.zhongyun@gmail.com

# These authors contributed equally to this work.

* To whom correspondence should be addressed.

Received November 3, 2013; Revision received December 9, 2013
Emerging data have shown that microRNAs (miRNAs) have important functions in the processes of cardiac hypertrophy and heart failure that occur during the postnatal period. Cardiac overexpression of miR-195 results in pathological cardiac growth and heart failure in transgenic mice. In the present study, we analyzed the roles of miR-195 in cardiomyocyte hypertrophy and found that miR-195 was greatly upregulated during isoprenaline-induced cardiomyocyte hypertrophy. By using mRNA microarray and molecular approach, we identified a novel putative target of miR-195 called high-mobility group A1 (HMGA1). Total mRNA microarray showed that HMGA1 was downregulated in primary cardiomyocytes that overexpressed miR-195. Using luciferase activity assay, we demonstrated that miR-195 interacts with the 3′-untranslated region of HMGA1 mRNA. Moreover, we showed that miR-195 in primary cardiomyocytes downregulates the expression of HMGA1 at the protein level. Taken together, our data demonstrated that miR-195 can negatively regulate a new target, HMGA1, which is involved in cardiomyocyte hypertrophy.
KEY WORDS: microRNA-195, cardiomyocyte hypertrophy, microRNA target, HMGA1

DOI: 10.1134/S0006297914060078