β-Catenin overexpression causes an increase in inflammatory cytokines and NF-kB activation in cardiomyocytes

β-Catenin has been implicated in various developmental and physiological processes. Defective Wnt signaling can result in different cardiac and vascular abnormalities and is activated under pathological conditions such as inflammation and obesity. In this study, roles of β-catenin in inflammation in cardiomyocytes were investigated. 10 samples from hearts of patients with acute infarction and 10 from normal ones were collected in order to access roles of β-catenin in cardiomyocytes. H9c2 cardiomyoblasts and primary neonatal rat cardiomyocytes were transfected with porcine cytomegalovirus (pCMV)-β-catenin plasmid in order to overexpress β-catenin. Protein level of β-catenin protein was increased in human acute infarction tissues compared to ones from normal patients. The transcription factor had increased nuclear localization in cardiomyocytes of the Wistar rats with cardiac hypertension. Furthermore, expression of fibrosis protein markers increased. Protein expression of β-catenin was increased in human acute infarction inflammatory heart tissues and in hearts of inflammatory obesity rats. After pCMV-β-catenin plasmid was transfected in a dose-dependent manner, inflammation protein markers, TNF-a and IL-8, were upregulated in hypertensive neonatal rat cardiomyocytes and H9c2 cardiomyoblasts. In addition, overexpression of β-catenin induced activation and nuclear localization of NF-kB. Therefore, β-catenin is a potential molecular target for treatment of inflammation and fibrosis in cardiomyocytes.