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

James C. Lin, Wei Wen Kuo, Rathinasamy Baskaran, Ming Cheng Chen, Tsung Jung Ho, Ray Jade Chen, Ya Fang Chen, Viswanadha Vijaya Padma, Ing Shiow Lay, Chih Yang Huang

Research output: Contribution to journalArticle

12 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)195-205
Number of pages11
JournalCardiology Journal
Volume24
Issue number2
DOIs
Publication statusPublished - 2017

Keywords

  • Apoptosis
  • Cardiomyocytes
  • Fibrosis
  • Survival pathway
  • β-catenin

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'Enhancement of beta-catenin in cardiomyocytes suppresses survival protein expression but promotes apoptosis and fibrosis'. Together they form a unique fingerprint.

Cite this