Therapeutic role of miR-19a/19b in cardiac regeneration and protection from myocardial infarction

Feng Gao, Masaharu Kataoka, Ning Liu, Tian Liang, Zhan-Peng Huang, Fei Gu, Jian Ding, Jianming Liu, Feng Zhang, Qing Ma, Yingchao Wang, Mingming Zhang, Xiaoyun Hu, Jan Kyselovic, Xinyang Hu, William T. Pu, Jian’an Wang, Jinghai Chen () and Da-Zhi Wang ()
Additional contact information
Feng Gao: Zhejiang University School of Medicine
Masaharu Kataoka: Harvard Medical School
Ning Liu: Zhejiang University School of Medicine
Tian Liang: Zhejiang University School of Medicine
Zhan-Peng Huang: Harvard Medical School
Fei Gu: Harvard Medical School
Jian Ding: Harvard Medical School
Jianming Liu: Harvard Medical School
Feng Zhang: Zhejiang University School of Medicine
Qing Ma: Harvard Medical School
Yingchao Wang: Zhejiang University School of Medicine
Mingming Zhang: Harvard Medical School
Xiaoyun Hu: Harvard Medical School
Jan Kyselovic: Comenius University
Xinyang Hu: Zhejiang University School of Medicine
William T. Pu: Harvard Medical School
Jian’an Wang: Zhejiang University School of Medicine
Jinghai Chen: Zhejiang University School of Medicine
Da-Zhi Wang: Harvard Medical School

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: Abstract The primary cause of heart failure is the loss of cardiomyocytes in the diseased adult heart. Previously, we reported that the miR-17-92 cluster plays a key role in cardiomyocyte proliferation. Here, we report that expression of miR-19a/19b, members of the miR-17-92 cluster, is induced in heart failure patients. We show that intra-cardiac injection of miR-19a/19b mimics enhances cardiomyocyte proliferation and stimulates cardiac regeneration in response to myocardial infarction (MI) injury. miR-19a/19b protected the adult heart in two distinctive phases: an early phase immediately after MI and long-term protection. Genome-wide transcriptome analysis demonstrates that genes related to the immune response are repressed by miR-19a/19b. Using an adeno-associated virus approach, we validate that miR-19a/19b reduces MI-induced cardiac damage and protects cardiac function. Finally, we confirm the therapeutic potential of miR-19a/19b in protecting cardiac function by systemically delivering miR-19a/19b into mice post-MI. Our study establishes miR-19a/19b as potential therapeutic targets to treat heart failure.

Date: 2019
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DOI: 10.1038/s41467-019-09530-1

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