Abstract:
: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 p38β 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.
journal_name
Mol Cell Biochemjournal_title
Molecular and cellular biochemistryauthors
Weng YJ,Kuo WW,Kuo CH,Tung KC,Tsai CH,Lin JA,Tsai FJ,Hsieh DJ,Huang CY,Hwang JMdoi
10.1007/s11010-010-0578-3subject
Has Abstractpub_date
2010-12-01 00:00:00pages
241-7issue
1-2eissn
0300-8177issn
1573-4919journal_volume
345pub_type
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