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Long noncoding RNA Meg3 regulates cardiomyocyte apoptosis in myocardial infarction

Hongchun Wu1,2, Zhen-Ao Zhao1,2, Junwei Liu3

  • 1Institute for Cardiovascular Science & Department of Cardiovascular Surgery of the First Affiliated Hospital, Medical College, Soochow University, Suzhou, 215000, China.

Gene Therapy
|October 6, 2018
PubMed

Insights

Long non-coding RNA Meg3 promotes heart cell death after myocardial infarction (MI). Knocking down Meg3 improves cardiac function in mice, offering a potential new treatment strategy for MI.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Genetics

Background:

  • Myocardial infarction (MI) is a major cause of death globally, characterized by cardiomyocyte death.
  • Long non-coding RNAs (lncRNAs) are implicated in cardiovascular diseases, but their specific roles in MI-induced cardiomyocyte death require further investigation.

Purpose of the Study:

  • To investigate the role of the lncRNA Meg3 in regulating cardiomyocyte apoptosis following myocardial infarction.
  • To explore the therapeutic potential of targeting Meg3 in MI treatment.

Main Methods:

  • Assessed Meg3 expression in mouse hearts post-MI.
  • Utilized gain-of-function and loss-of-function studies in rodent cardiomyocytes.
  • Investigated the regulatory relationship between Meg3, p53, and FUS.
  • Employed adeno-associated virus serotype 9 (AAV9) for in vivo gene knockdown in MI mice.
  • Analyzed Meg3 expression in human heart failure samples and human cardiomyocytes.

Main Results:

  • Meg3 expression was progressively upregulated in mouse hearts after MI.
  • Meg3 exhibited pro-apoptotic functions in cardiomyocytes.
  • p53 directly upregulated Meg3 under hypoxic conditions, and Meg3 bound to FUS to regulate apoptosis.
  • Knockdown of Meg3 using AAV9 improved cardiac function in adult MI mice.
  • MEG3 levels were elevated in clinical heart failure samples and demonstrated conserved pro-apoptotic effects in human cardiomyocytes.

Conclusions:

  • The p53-induced Meg3-FUS complex plays a significant role in cardiomyocyte apoptosis post-MI.
  • Targeted knockdown of Meg3 using an AAV9 system is a promising preclinical strategy for treating myocardial infarction.

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