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MicroRNA-30b-5p Is Involved in the Regulation of Cardiac Hypertrophy by Targeting CaMKIIδ
  1. Juan He, MS,
  2. Shan Jiang, MS,
  3. Feng-lan Li, MS,
  4. Xue-jiao Zhao, MS,
  5. Er-fu Chu, MS,
  6. Mei-na Sun, MS,
  7. Ming-zi Chen, MS,
  8. Hui Li, PhD
  1. From the Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China.
  1. Received April 24, 2012, and in revised form November 6, 2012.
  2. Accepted for publication November 8, 2012.
  3. Reprints: Hui Li, PhD, Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, China. E-mail: lihuiteacher{at}
  4. Supported by National Natural Science Foundation of China Grants 30771863 and 81172616, and Excellent Academic Leaders Foundation of Harbin Science and Technology Agency of China Grant 2008RFXXS019.


Background MicroRNAs (miRNAs) participate in the regulation of cardiac hypertrophy. However, it remains largely unknown as to how miRNAs are integrated into the hypertrophic program. Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a hypertrophic signaling marker. It is not yet clear which miRNAs can regulate CaMKIIδ.

Purpose In this study, we identified which miRNAs could regulate CaMKIIδ and how to regulate CaMKIIδ.

Methods Through computational and expression analyses, miR-30b-5p was identified as a candidate regulator of CaMKIIδ. Quantitative expression analysis of hypertrophic models demonstrated significant down-regulation of miR-30b-5p compared with control groups. Luciferase reporter assay showed that miR-30b-5p could significantly inhibit the expression of CaMKIIδ. Moreover, through gain-of-function and loss-of-function approaches, we found miR-30b-5p could negatively regulate the expression of CaMKIIδ and miR-30b-5p was a regulator of cardiac hypertrophy.

Conclusion Our study demonstrates that the expression of miR-30b-5p is down-regulated in cardiac hypertrophy, and restoration of its function inhibits the expression of CaMKIIδ, suggesting that miR-30b-5p may act as a hypertrophic suppressor.

Key Words
  • cardiac hypertrophy
  • CaMKIIδ
  • miR-30b-5p
  • isoproterenol

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