期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 295, 期 4, 页码 937-944出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S0006-291X(02)00789-1
关键词
TNF-alpha; chondrocyte; apoptosis; actinomycin D; proteasome inhibitor; NF-kappa B
The mechanism of TNF-alpha-mediated chondrocyte apoptosis in human articular cartilage was investigated. First passage OA chondrocytes were treated with actinomycin D or MG132 in combination with TNF-alpha to facilitate cell death. The patterns of apoptosis-related proteins. NF-kappaB activation, and IkappaB degradation were analyzed. Cell death was increased by 0.2 mug/ml of actinomycin D or 20 muM MG132 in combination with TNF-alpha. Apoptosis potentiated by MG132 was more effectively inhibited by caspase inhibitors than that by actinomycin D. MG132 or actinomycin D both led to a significant increase in p53, but the expressions of the p53 response proteins increased only in MG132 treated chondrocytes. TNF-alpha induced chondrocyte IkappaB phosphorylation was unaffected by either MG132 or actinomycin D. MG132, but not actinomycin D, inhibited the chondrocyte IkappaB degradation induced by TNF-alpha and NF-kappaB activation. Our results suggest that MG132 and actinomycin D exert different influences upon TNF-alpha-mediated chondrocyte apoptotic signaling. (C) 2002 Elsevier Science (USA). All rights reserved.
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