|
|||||
|
|
BNIP3 induces IL6 and calcineurin/NFAT3 hypertrophic-related pathways in H9c2 cardiomyoblast cells |
|
| Authors: | Yi-Jiun Weng Wei-Wen Kuo Chia-Hua Kuo Kwong-Chung Tung Chang-Hai Tsai James A. Lin Fuu-Jen Tsai Dennis Jine-Yuan Hsieh Chih-Yang Huang Jin-Ming Hwang |
| Affiliation: | 1. Department of Veterinary Medicine, National Chung-Hsing University, Taichung 402, Taiwan, ROC 2. Department of Biological Science and Technology, China Medical University, Taichung 404, Taiwan, ROC 3. Laboratory of Exercise Biochemistry, Taipei Physical Education College, Taipei 105, Taiwan, ROC 4. Department of Healthcare Administration, Asia University, Taichung, Taiwan, ROC 5. Graduate Institute of Basic Medical Science, Taichung, Taiwan, ROC 6. Department of Chinese Medicine, China Medical University, Taichung 404, Taiwan, ROC 7. School of Medical Technology, Chung Shan Medical University, Taichung 402, Taiwan, ROC 8. Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan, ROC 9. School of Applied Chemistry, Chung Shan Medical University, No. 110, Section?1, Jianguo N. Road, Taichung 402, Taiwan, ROC |
| 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. |
| Keywords: | |
| 本文献已被 SpringerLink 等数据库收录！ | |