Hypoxia Augments Increased HIF-1 alpha and Reduced Survival Protein p-Akt in Gelsolin (GSN)-Dependent Cardiomyoblast Cell Apoptosis

doi:10.1007/s12013-016-0729-6

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Title:	Hypoxia Augments Increased HIF-1 alpha and Reduced Survival Protein p-Akt in Gelsolin (GSN)-Dependent Cardiomyoblast Cell Apoptosis
Authors:	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
Contributors:	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
Keywords:	Gelsolin Hypoxia p-Akt HIF-1 alpha Cardiomyoblast cell apoptosis
Date:	2016-06
Issue Date:	2018-01-18 11:39:38 (UTC+8)
Publisher:	Humana Press Inc
Abstract:	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.
Relation:	Cell Biochemistry and Biophysics, v.74 n.2, pp.221-228
Appears in Collections:	[Dept. of Hospital and Health (including master's program)] Periodical Articles

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