Enhancement of beta-catenin in cardiomyocytes suppresses survival protein expression but promotes apoptosis and fibrosis

Cardiol J. 2017;24(2):195-205. doi: 10.5603/CJ.a2016.0087. Epub 2016 Oct 13.

Abstract

Background: Beta-catenin has been implicated in cell-cell communication in a wide variety of developmental and physiological processes. Defective Wnt signaling could result in various cardiac and vascular abnormalities. Little is known regarding Wnt/frizzled pathway in cardiomyocyte apoptosis.

Methods: In this study, the role of b-catenin in apoptosis was investigated in H9c2 cardiomyocytes and primary cardiomyocytes isolated in diabetic Wistar rats. The cardiomyocytes were transfected with porcine cytomegalovirus (pCMV)-b-catenin plasmid in order to overexpress b-catenin.

Results: The transcription factor displayed a significant nuclear localization in Wistar rats with cardiac hypertension. Transfection of b-catenin plasmid induced apoptosis and reduced expression of survival pathway markers in cardiomyocytes in a dose-dependent manner. Furthermore, expression of fibrosis protein markers was upregulated by the overexpression.

Conclusions: Taken together, these results revealed that altered Wnt/b-catenin signaling might provoke heart failure. (Cardiol J 2017; 24, 2: 195-205).

Keywords: apoptosis; b-catenin; cardiomyocytes; fibrosis; survival pathway.

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Animals
  • Animals, Newborn
  • Apoptosis*
  • Blotting, Western
  • Cardiomyopathies / genetics*
  • Cardiomyopathies / metabolism
  • Cardiomyopathies / pathology
  • Cell Survival
  • Cells, Cultured
  • Diabetes Mellitus, Experimental
  • Gene Expression Regulation, Developmental*
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Myocytes, Cardiac / metabolism*
  • Myocytes, Cardiac / pathology
  • Rats
  • Rats, Wistar
  • Signal Transduction
  • Swine
  • beta Catenin / biosynthesis
  • beta Catenin / genetics*

Substances

  • beta Catenin