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Histone Deacetylase 1 Depletion Alleviates Coronary Heart Disease Via the MicroRNA-182-Mediated Transforming Growth

Shengkai Zhou1, Peng Liu, Guobao Zhang

  • 1Department of Cardiovascular Surgery, Fuwai Central China Cardiovascular Hospital, The People's Hospital of Zhengzhou University, Henan Provincial People's Hospital, Zhengzhou, Henan, P.R. China.

Journal of Cardiovascular Pharmacology
|March 15, 2022
PubMed

Insights

Histone deacetylase 1 (HDAC1) worsens coronary heart disease (CHD) by repressing miR-182, which activates the TGF-β/Smad pathway. Downregulating HDAC1 improves cardiac function and reduces injury in CHD rats.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Epigenetics

Background:

  • Histone deacetylases (HDACs) regulate gene expression by controlling histone acetylation.
  • HDAC inhibitors have shown potential in suppressing cardiomyocyte growth.
  • The specific role of HDAC1 in coronary heart disease (CHD) progression requires further investigation.

Purpose of the Study:

  • To investigate the role of HDAC1 in the pathogenesis of coronary heart disease (CHD).
  • To elucidate the regulatory mechanism of HDAC1 on microRNA-182 (miR-182) expression.
  • To determine the impact of the HDAC1/miR-182 axis on the transforming growth factor (TGF)-β/Smad pathway in CHD.

Main Methods:

  • Epigenetic probe array and chromatin immunoprecipitation for HDAC1 and miR-182 analysis.
  • MicroRNA microarray to identify downstream targets of HDAC1.
  • In vivo studies in CHD rats using various biochemical and histological assays.
  • Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and Western blot.

Main Results:

  • HDAC1 was overexpressed in CHD patients and repressed miR-182 expression in rat cardiomyocytes via deacetylation.
  • Downregulation of HDAC1 improved cardiac function, normalized lipid profiles, and reduced myocardial injury and inflammation in CHD rats.
  • miR-182 downregulation exacerbated cardiac injury in the context of HDAC1 knockdown.
  • HDAC1/miR-182 modulated the TGF-β/Smad pathway, with HDAC1 activating it and miR-182 inhibiting it.

Conclusions:

  • HDAC1 plays a crucial role in promoting CHD by repressing miR-182 expression.
  • The HDAC1-mediated repression of miR-182 leads to the activation of the TGF-β/Smad pathway, contributing to CHD progression.
  • Targeting the HDAC1/miR-182 axis presents a potential therapeutic strategy for managing coronary heart disease.

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