Original Paper

Journal of Molecular Histology

, Volume 44, Issue 5, pp 565-573

First online:

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

  • Qiaoli ZhengAffiliated withDepartment of Pathology, Sun Yat-sen University the Fifth Affiliated Hospital
  • , Ping ChenAffiliated withDepartment of Pathology, Jiangmen Central Hospital
  • , Zeqing XuAffiliated withDepartment of Pathology, Sun Yat-sen University the Fifth Affiliated Hospital
  • , Faqian LiAffiliated withDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center
  • , Xian Ping YiAffiliated withDepartment of Pathology, Sun Yat-sen University the Fifth Affiliated Hospital Email author 

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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.

Keywords

Cardiac hypertrophy Beta-catenin Cadherin Glycogen synthase kinase-3β (GSK3β) Signal transduction