Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 345, Issue 1-2, Pages 241-247Publisher
SPRINGER
DOI: 10.1007/s11010-010-0578-3
Keywords
BNIP3; Hypertrophy; NFAT3; IL6; H9c2 cardiomyoblast cells
Categories
Funding
- Taiwan Department of Health Clinical Trial and Research Center of Excellence [DOH99-TD-B-111-004]
- Taiwan Department of Health Cancer Research Center of Excellence [DOH99-TD-C-111-005]
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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.
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