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

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.

Keywords: GATA4; Hypertrophy; Infarction; NFATc3; β-Catenin.