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MiR-449 improves cardiac function by regulating HDAC1 and cTnI.

B Yang1, H Zhao, R Dong

  • 1Department of Cardiology, Chinese PLA General Hospital, Beijing, China. FengCaofengrao@163.com.

European Review for Medical and Pharmacological Sciences
|December 30, 2020
PubMed
Summary

MicroRNA-449 (miRNA-449) enhances cardiac function by upregulating cardiac troponin I (cTnI) expression. It achieves this by inhibiting Histone deacetylase 1 (HDAC1), promoting histone acetylation, and facilitating transcription factor GATA4 binding to the cTnI promoter.

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Epigenetics

Background:

  • Cardiac troponin I (cTnI) is crucial for cardiac function.
  • Dysregulation of cTnI expression is linked to cardiac dysfunction.
  • MicroRNAs (miRNAs) play significant roles in cardiovascular regulation.

Purpose of the Study:

  • To investigate the role of microRNA-449 (miRNA-449) in regulating cTnI expression and cardiac function.
  • To elucidate the mechanism involving Histone deacetylase 1 (HDAC1)-mediated histone deacetylation in cardiomyocytes.

Main Methods:

  • Biochemical analysis and Dual-Luciferase reporter gene assays were used to confirm interactions.
  • In vivo studies in elderly mice with low cTnI expression were conducted using miRNA-449 agomiR intervention.

Main Results:

  • miRNA-449 directly interacts with HDAC1.
  • HDAC1-mediated histone deacetylation of H3K4 and H3K9 in the cTnI promoter region regulates cTnI gene expression.
  • HDAC1 inhibition by miRNA-449 improved cardiac function in elderly mice.

Conclusions:

  • miRNA-449 upregulates cTnI gene expression by modulating histone acetylation at the cTnI promoter.
  • This process involves the recruitment of transcription factor GATA4.
  • miRNA-449-mediated upregulation of cTnI improves cardiac function in aged mice with low cTnI levels.