Increased β-catenin accumulation and nuclear translocation are associated with concentric hypertrophy in cardiomyocytes

Cheng Yu Lee, Wei Wen Kuo, Rathinasamy Baskaran, Cecilia Hsuan Day, Pei Ying Pai, Chao Hung Lai, Yu Feng Chen, Ray Jade Chen, Viswanadha Vijaya Padma, Chih Yang Huang

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Defective Wnt/β-Catenin signaling, activated under various pathological conditions, can result in cardiac and vascular abnormalities. In the present study, the possible role of β-catenin over expression during cardiac hypertrophy was investigated. Ten samples from hearts of human patients with acute infarction, and granulation tissue from 20 patients and 10 from normal ones were collected in order to investigate roles of β-catenin in cardiac hypertrophy. H9c2 cardiomyoblast cells and Wistar rat primary neonatal cardiomyocytes were overexpressed with β-catenin. Expression levels of β-catenin protein were increased in human acute infarction tissues and rat hypertension heart tissues. Overexpression of this transcription factor induced actin filament formation and increased hypertrophic marker protein levels via MAPK pathway. In addition, β-catenin overexpression also resulted in increased elevation of NFATc3 and p-GATA4. Therefore, acute infarction resulted in β-catenin overexpression mediated hypertrophy in cardiomyocytes regulated through MAPK pathway.

Original languageEnglish
Pages (from-to)9-16
Number of pages8
JournalCardiovascular Pathology
Volume31
DOIs
Publication statusPublished - Nov 1 2017

Keywords

  • GATA4
  • Hypertrophy
  • Infarction
  • NFATc3
  • β-Catenin

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Cardiology and Cardiovascular Medicine

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    Lee, C. Y., Kuo, W. W., Baskaran, R., Day, C. H., Pai, P. Y., Lai, C. H., Chen, Y. F., Chen, R. J., Padma, V. V., & Huang, C. Y. (2017). Increased β-catenin accumulation and nuclear translocation are associated with concentric hypertrophy in cardiomyocytes. Cardiovascular Pathology, 31, 9-16. https://doi.org/10.1016/j.carpath.2017.07.003