S-Space College of Medicine/School of Medicine (의과대학/대학원) Pediatrics (소아과학전공) Journal Papers (저널논문_소아과학전공)
Effect of chronic hypoxia on proliferation, apoptosis, and HSP70 expression in mouse bronchiolar epithelial cells
- Kim, Ee-Kyung; Park, June Dong; Shim, So-Yeon; Kim, Han-Suk; Kim, Beyong Il; Choi, Jung-Hwan; Kim, Ji Eun
- Issue Date
- Physiol Res. 2006;55(4):405-11. Epub 2005 Oct 17.
- Anoxia/metabolism/*pathology/*physiopathology; Apoptosis/*physiology; Animals; Blotting, Western; Bronchi/metabolism/pathology/physiopathology; Cell Division/physiology; Chronic Disease; Epithelial Cells/metabolism/pathology; Gene Expression Regulation/physiology; HSP70 Heat-Shock Proteins/*genetics/metabolism; Immunohistochemistry; In Situ Nick-End Labeling; Ki-67 Antigen/metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Respiratory Mucosa/metabolism/*pathology/physiopathology
- Heat shock proteins (HSPs) can be induced by various stresses and play an important role in cell cycle progression. HSP70 has been shown to act as an inhibitor of apoptosis. We studied HSP70 expression in bronchial epithelial cells of C57BL/6 mice and homozygous HPS70 knockout mice (hsp70.1-/-) exposed to chronic hypoxic stress. We also investigated changes in cellular proliferation and apoptosis in relation to HSP70. Lungs were removed from mice after a three-week period of exposure to 10 % O(2). Immunoblots for HSP70 and immunohistochemical staining for HSP70 and Ki-67 were performed. Apoptosis was assessed using the TUNEL assay. The three-week period of hypoxic stress did not change HSP70 levels in total lung tissue, but a significant reduction in HSP70 expression was observed in bronchiolar epithelial cells. In wild type mice, both HSP70 and Ki-67 expression were significantly reduced in bronchiolar epithelial cells. In homozygous HPS70 knockout mice (hsp70.1-/-), apoptosis of bronchiolar epithelial cells was significantly increased. Our results suggest that HSP70 may exert anti-apoptotic effects in mouse bronchiolar epithelial cells.
- 0862-8408 (Print)
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