Effect of Chronic Hypoxia on
Proliferation, Apoptosis, and HSP70 Expression in Mouse
Bronchiolar Epithelial Cells
E-K. KIM, J.D. PARK, S-Y. SHIM, H-S. KIM, B.I.
KIM, J-H. CHOI, J.E. KIM1
Department of Pediatrics, 1Department of Pathology, Seoul
National University College of Medicine, Seoul, Korea
Received February 22, 2005
Accepted August 10, 2005
On-line available October 17, 2005
Summary
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 %
O2. 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.
Key words
Chronic hypoxia • Bronchiolar epithelium • HSP70 • Proliferation
• Apoptosis
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