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標題: BNIP3 induces IL6 and calcineurin/NFAT3 hypertrophic-related pathways in H9c2 cardiomyoblast cells
作者: Weng, Y.J.
Kuo, W.W.
Kuo, C.H.
Tung, K.C.
Tsai, C.H.
Lin, J.A.
Tsai, F.J.
Hsieh, D.J.Y.
Huang, C.Y.
Hwang, J.M.
關鍵字: BNIP3;Hypertrophy;NFAT3;IL6;H9c2 cardiomyoblast cells;eccentric cardiac-hypertrophy;malignant glioma-cells;jak stat pathway;gene-expression;signaling pathways;pressure-overload;protein bnip3;bh3 domain;kinase;mitochondrial
Project: Molecular and Cellular Biochemistry
期刊/報告no:: Molecular and Cellular Biochemistry, Volume 345, Issue 1-2, Page(s) 241-247.
Ischemia/reperfusion injury causes cardiomyocyte apoptosis, ventricular remodeling, leading to a dilated heart. Hypoxia is one of the causes involved in ischemia damage, and BNIP3 is a hypoxia-inducible marker and also a sensor to induce mitochondria-dependent apoptosis. Recent reports discussed ablating BNIP3 can restrain cardiomyocytes apoptosis and post-infarction remodeling. BNIP3 is a crucial therapeutic target. However, the BNIP3-induced hypertrophy aspect is rarely investigated. Here, we transiently transfected BNIP3 plasmids into H9c2 cardiomyoblast cells to evaluate the molecular signaling and hypertrophy markers using Western blot. We measured the cell size change using actin staining. We disclose that BNIP3 overexpression induced an increase in cell size, activated the pathological-related hypertrophy signaling pathways, such as IL6-MEK5-ERK5, IL6-JAK2-STAT1/3, calcineurin/NFAT3 and p38 beta MAPK resulting in the fetal genes, ANP and BNP expressing. Concluding above, BNIP3 acts as a pathological hypertrophy inducer, which might be a potential therapeutic target for heart damage prevention.
ISSN: 0300-8177
DOI: 10.1007/s11010-010-0578-3
Appears in Collections:獸醫學系所

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