Expression and redistribution of β-catenin in the cardiac myocytes of left ventricle of spontaneously hypertensive rat

Abstract

Beta-catenin is not only an adhering junction protein, but also the central player of the canonical Wnt signalling pathway. In order to investigate the roles of β-catenin in the mechanism of myocardial hypertrophy, we determined the expression and distribution of β-catenin in the cardiomyocytes of spontaneously hypertensive heart failure (SHHF) rats and age-matched Wistar-Kyoto (WKY) rats. We identified the reducing of β-catenin expression in the membrane protein fraction but increasing in the nuclear protein in the 6 and 12 month-old SHHF rats as compared with the age-matched WKY rats by Western blotting. Immunolabeling of β-catenin colocalized with cadherin at the intercalated disc sites and showed nuclear accumulation in myocytes of SHHF rats. We also revealed that the association between glycogen synthase kinase-3β and β-catenin had weakened in the 6 month-old SHHF rats as compared with the age-matched WKY rats by immunoprecipitation. These findings suggested that nuclear translocation of β-catenin might play important roles in regulating signal transduction in the decompensated hypertrophy stage.

Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling

“…A study by Zheng et al [26] implicated β-catenin in the pathophysiology of hypertension, which is the main risk factor of LVH in clinical settings [2]. Clinical and experimental studies have shown that the renin-ANG-aldosterone system (RAAS) is over-activated in cardiac hypertrophy and heart failure [31].…”

“…Conversely, conditional deletion of the β-catenin gene significantly reduced the hypertrophic responses of animals [12]. Furthermore, Zheng and colleagues [26] reported the nuclear localization of β-catenin in ventricles of hypertensive rats. Aspirin reportedly inhibits Wnt/β-catenin signaling in cancer cells [9], and β-catenin expression can be activated by ANG II exposure [27].…”

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

“…Beta-catenin signaling is activated during pathological cardiac remodeling induced by pressure overload in injured arteries and after myocardial infarction [14]. In addition, it was found to induce apoptosis in other mammalian cell types [16][17][18], heart failure in rats [19] and cardiac fibrosis [20]. However, the role of b-catenin in apoptosis, fibrosis and survival in cardiomyocytes requires further study.…”

“…1A). In previous studies, the authors observed cardiac fibrosis and apoptosis in a diabetic animal model [19,31]. In addition, b-catenin protein expression in diseased animal models was determined.…”

“…In other mammalian cell types, overexpression of b-catenin promotes apoptosis [16][17][18]. In a previous study, it was demonstrated that b-catenin was increased in cardiomyocytes of spontaneously hypertensive heart failure in rats compared with an age-matched control group [19]. In another study, it was indicated that when heart injury occurs, Wnt signaling activates and induces cardiac fibrosis [20].…”