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Cardiac expression of microRNA-7 is associated with adverse cardiac remodeling

Manveen K Gupta1, Anita Sahu2, Yu Sun2

  • 1Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH, 44195, USA. manveenkgupta@yahoo.com.

Scientific Reports
|November 11, 2021
PubMed

Insights

microRNA-7 (miRNA-7) overexpression in heart cells causes cardiac dilation and fibrosis, not adaptive hypertrophy. This suggests miRNA-7 has a novel role in cardiac function beyond regulating EGFR/ERBB family members.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Genetics

Background:

  • microRNA-7 (miRNA-7) is recognized for regulating cancer cell proliferation via the Epidermal growth factor receptor (EGFR/ERBB) family.
  • Its specific role in cardiac physiology and pathology remains largely uncharacterized.

Purpose of the Study:

  • To investigate the function of miRNA-7 in cardiac physiology and pathology.
  • To determine the effects of cardiomyocyte-specific miRNA-7 overexpression in transgenic (Tg) mouse models.

Main Methods:

  • Generation of cardiomyocyte-specific miRNA-7 Tg mice.
  • Echocardiography to assess cardiac function and structure.
  • Transverse aortic constriction (TAC) model to induce cardiac stress.
  • Analysis of ERBB2 and ERBB1 (EGFR) expression.
  • Cardiac proteomics and electron microscopy to evaluate mitochondrial structure and function.

Main Results:

  • miRNA-7 Tg mice exhibited cardiac dilation instead of physiological hypertrophy.
  • TAC induced cardiac dilation and fibrosis in miRNA-7 Tg mice, bypassing adaptive hypertrophy.
  • miRNA-7 overexpression led to reduced ERBB2 expression but not ERBB1 (EGFR).
  • Proteomics revealed decreased mitochondrial membrane proteins, and electron microscopy showed disorganized mitochondria with impaired function.

Conclusions:

  • Cardiomyocyte-specific miRNA-7 expression causes cardiac dilation and fibrosis, impairing adaptive hypertrophic responses to aging and stress.
  • miRNA-7 influences cardiac function through mechanisms beyond EGFR/ERBB regulation, involving mitochondrial integrity and function.

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