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    標題: beta-Catenin overexpression causes an increase in inflammatory cytokines and NF-kappa B activation in cardiomyocytes
    作者: Lin, J. C.
    Chang, R-L.
    Chen, Y-F.
    Yang, J-J.
    Baskaran, R.
    Chung, L-C.
    Chen, R-J.
    Day, C. H.
    Padma, V. Vijaya
    Huang, C-Y.
    貢獻者: Asia Univ, Dept Occupat Therapy
    Cheng Ching Hosp, Dept Internal Med
    China Med Univ, Coll Chinese Med, Sch Postbaccalaureate Chinese Med
    China Med Univ, Grad Inst Chinese Med
    Taichung Vet Gen Hosp, Dept Obstet & Gynecol
    Chung Shan Med Univ, Coll Oral Med, Inst Oral Sci
    China Med Univ, Grad Inst Basic Med Sci
    Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm
    Taipei Med Univ, Coll Med, Sch Med, Dept Surg
    MeiHo Univ, Dept Nursing
    Bharathiar Univ, Dept Biotechnol
    Asia Univ, Dept Hlth & Nutr Biotechnol
    關鍵字: Acute infarction
    H9c2 cardiomyocytes
    beta-catenin
    inflammation
    NF-kappa B
    日期: 2017
    上傳時間: 2018-11-30 15:50:15 (UTC+8)
    出版者: C M B Assoc
    摘要: beta-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 beta-catenin in inflammation in cardio-myocytes were investigated. 10 samples from hearts of patients with acute infarction and 10 from normal ones were collected in order to access roles of beta-catenin in cardiomyocytes. H9c2 cardiomyoblasts and primary neonatal rat cardiomyocytes were transfected with porcine cytomegalovirus (pCMV)-beta-catenin plasmid in order to overexpress beta-catenin. Protein level of beta-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 beta-catenin was increased in human acute infarction inflammatory heart tissues and in hearts of inflammatory obesity rats. After pCMV-beta-catenin plasmid was transfected in a dose-dependent manner, inflammation protein markers, TNF-alpha and IL-8, were upregulated in hypertensive neonatal rat cardiomyocytes and H9c2 cardiomyoblasts. In addition, overexpression of beta-catenin induced activation and nuclear localization of NF-.B. Therefore, beta-catenin is a potential molecular target for treatment of inflammation and fibrosis in cardiomyocytes.
    關聯: Cellular and Molecular Biology, v.63, n.1, pp.17-22
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