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

Author

Listed:
  • Feng Gao

    (Zhejiang University School of Medicine)

  • Masaharu Kataoka

    (Harvard Medical School
    Keio University School of Medicine)

  • Ning Liu

    (Zhejiang University School of Medicine)

  • Tian Liang

    (Zhejiang University School of Medicine)

  • Zhan-Peng Huang

    (Harvard Medical School
    Sun Yat-sen University)

  • 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
    Harvard University)

  • Jian’an Wang

    (Zhejiang University School of Medicine)

  • Jinghai Chen

    (Zhejiang University School of Medicine)

  • Da-Zhi Wang

    (Harvard Medical School
    Harvard University)

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.

Suggested Citation

  • 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, 2019. "Therapeutic role of miR-19a/19b in cardiac regeneration and protection from myocardial infarction," Nature Communications, Nature, vol. 10(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-09530-1
    DOI: 10.1038/s41467-019-09530-1
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    Cited by:

    1. Xueqiang Wang & Xing Zhang & Ke Cao & Mengqi Zeng & Xuyang Fu & Adi Zheng & Feng Zhang & Feng Gao & Xuan Zou & Hao Li & Min Li & Weiqiang Lv & Jie Xu & Jiangang Long & Weijin Zang & Jinghai Chen & Fen, 2022. "Cardiac disruption of SDHAF4-mediated mitochondrial complex II assembly promotes dilated cardiomyopathy," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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