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| 標題: | Hypoxia Augments Increased HIF-1 alpha and Reduced Survival Protein p-Akt in Gelsolin (GSN)-Dependent Cardiomyoblast Cell Apoptosis |
| 作者: | Yeh, Yu-Lan
Ting, Wei-Jen
Shen, Chia-Yao
Hsu, Hsi-Hsien
Chung, Li-Chin
Tu, Chuan-Chou
Chang, Sheng-Huang
Day, Cecilia-Hsuan
Tsai, Yuhsin
Huang, Chih-Yang |
| 貢獻者: | Changhua Christian Hosp, Dept Pathol
Jen Teh Jr Coll Med Nursing & Management, Dept Med Technol
China Med Univ & Hosp, Sch Chinese Med
MeiHo Univ, Dept Nursing
Mackay Mem Hosp, Div Colorectal Surg
Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm, Tainan, Tainan County, Taiwan
Armed Force Taichung Gen Hosp, Dept Internal Med, Div Chest Med
Tsao Tun Psychiat Ctr, Dept Hlth
China Med Univ, Sch Chinese Med
Asia Univ, Dept Hlth & Nutr Biotechnol |
| 關鍵字: | Gelsolin
Hypoxia
p-Akt
HIF-1 alpha
Cardiomyoblast cell apoptosis |
| 日期: | 2016-06 |
| 上傳時間: | 2018-01-18 11:39:38 (UTC+8) |
| 出版者: | Humana Press Inc |
| 摘要: | Cytoskeleton filaments play an important role in cellular functions such as maintaining cell shape, cell motility, intracellular transport, and cell division. Actin-binding proteins (ABPs) have numerous functions including regulation of actin filament nucleation, elongation, severing, capping, cross linking, and actin monomer sequestration. Gelsolin (GSN) is one of the actin-binding proteins. Gelsolin (GSN) is one of the actin-binding proteins that regulate cell morphology, differentiation, movement, and apoptosis. GSN also regulates cell morphology, differentiation, movement, and apoptosis. In this study, we have used H9c2 cardiomyoblast cell and H9c2-GSN stable clones to understand the roles and mechanisms of GSN overexpression in hypoxia-induced cardiomyoblast cell death. The data show that hypoxia or GSN overexpression induces HIF-1 alpha expression and reduces the expression of survival markers p-Akt and Bcl-2 in H9c2 cardiomyoblast cells. Under hypoxic conditions, GSN overexpression further reduces p-Akt expression and elevates total as well as cleaved GSN levels and HIF-1 alpha levels. In addition, GSN overexpression enhances apoptosis in cardiomyoblasts under hypoxia. Hypoxic challenge further induced activated caspase-3 and cell death that was attenuated after GSN knock down, which implies that GSN is a critical therapeutic target against hypoxia-induced cardiomyoblast cell death. |
| 關聯: | Cell Biochemistry and Biophysics, v.74 n.2, pp.221-228 |
| 顯示於類別: | [醫務管理系(所)] 期刊論文
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