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- Title
Hypoxia Augments Increased HIF-1α 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
- 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-1α 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-1α 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.
- Subjects
HYPOXEMIA; PROTEINS; GELSOLIN; CELL differentiation; CELL morphology
- Publication
Cell Biochemistry & Biophysics, 2016, Vol 74, Issue 2, p221
- ISSN
1085-9195
- Publication type
Article
- DOI
10.1007/s12013-016-0729-6