Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/32988
標題: BNIP3 induces IL6 and calcineurin/NFAT3 hypertrophic-related pathways in H9c2 cardiomyoblast cells
作者: Weng, Y.J.
董光中
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
期刊/報告no:: Molecular and Cellular Biochemistry, Volume 345, Issue 1-2, Page(s) 241-247.
摘要: 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.
URI: http://hdl.handle.net/11455/32988
ISSN: 0300-8177
文章連結: http://dx.doi.org/10.1007/s11010-010-0578-3
Appears in Collections:獸醫學系所

文件中的檔案:

取得全文請前往華藝線上圖書館



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.