Abstract
Cardiovascular diseases have a high prevalence worldwide and constitute the leading causes of mortality. Recently, malfunctioning of β-catenin signaling has been addressed in hypertensive heart condition. Ang-II is an important mediator of cardiovascular remodeling processes which not only regulates blood pressure but also leads to pathological cardiac changes. However, the contribution of Ang-II/β-catenin axis in hypertrophied hearts is ill-defined. Employing in vitro H9c2 cells and in vivo spontaneously hypertensive rats (SHR) cardiac tissue samples, western blot analysis, luciferase assays, nuclear-cytosolic protein extracts, and immunoprecipitation assays, we found that under hypertensive condition β-catenin gets abnormally induced that co-activated LEF1 and lead to cardiac hypertrophy changes by up-regulating the IGF-IIR signaling pathway. We identified putative LEF1 consensus binding site on IGF-IIR promoter that could be regulated by β-catenin/LEF1 which in turn modulate the expression of cardiac hypertrophy agents. This study suggested that suppression of β-catenin expression under hypertensive condition could be exploited as a clinical strategy for cardiac pathological remodeling processes.
Highlights
Global prevalence of cardiovascular diseases has been on the rise and constitutes the leadingGlobal prevalence of cardiovascular diseases has been on the rise and constitutes the leading causes of death worldwide [1]
Prolonged cardiac stresses may lead to stresses may lead to irreversible cardiac hypertrophic responses that may result in the development irreversible cardiac hypertrophic responses that may result in the development of pathological cardiac of pathological cardiac structural and functional changes which may culminate into heart failure
We examined the impact of β-catenin in angiotensin II (Ang-II) induced hypertrophy responses and demonstrated that IGF-IIR expression could be regulated by β-catenin/LEF1 leading to pathological cardiac hypertrophy signaling
Summary
Global prevalence of cardiovascular diseases has been on the rise and constitutes the leading. Cardiac hypertrophy is an adaptive mechanism to enable un-interrupted un-interrupted healthier heart functions under stressful conditions. Our earlier studies have shown the involvement of IGF-IIR signaling in the development signaling in the development of pathological cardiac changes during stresses via of pathological cardiac changes during stresses via Gαq/PKCα/NFATC3 modulations [5,6]. The role of Ang-II/β-catenin axis in cardiac hypertrophy responses is not completely responses is not completely elucidated. As such it is worthwhile to investigate the precise mechanisms elucidated. As such it is worthwhile to investigate the precise mechanisms of interplay between of interplay between β-catenin/LEF1 signaling and Ang-II induced cardiac hypertrophy response.
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