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

---