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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2003-10-20
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pubmed:abstractText |
This study addresses mechanisms by which interleukin-1beta (IL-1beta) regulates human chondrocyte apoptosis induced by a combination of the anti-CD95 antibody CH-11 and the proteasome inhibitor (PSI). The effect of IL-1beta on apoptosis varied among tissue samples. IL-1beta either enhanced (16/22 samples) or inhibited (6/22 samples) DNA fragmentation and caspase-3 processing. The protective effect of IL-1beta was abrogated by the nitric oxide (NO) synthesis inhibitor N-monomethyl-l-arginine (L-NMMA) while apoptosis stimulation was not affected. The NO-donors sodium nitroprusside (SNP) and S-nitroso-N-acetyl penicillamine (SNAP) blocked DNA fragmentation, and this was associated with partial inhibition of caspase-3 processing. Pyrrolidine dithiocarbamate (PDTC), a scavenger of reactive oxygen species (ROS) blocked apoptosis induction by CH-11/PSI as well as the enhancement by IL-1beta. The pro-apoptotic effects of IL-1beta were also abrogated by the p38 inhibitor SB 202190. In conclusion, IL-1beta augments CH-11/PSI induced apoptosis in the majority of chondrocyte samples. The pro-apoptotic effect of IL-1beta is not dependent on NO. In contrast, the anti-apoptotic effect of IL-1beta observed in a minority of samples is partially NO-dependent.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/CASP3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Free Radical Scavengers,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Donors,
http://linkedlifedata.com/resource/pubmed/chemical/PSMF1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/omega-N-Methylarginine,
http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0021-9541
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
197
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
379-87
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:14566967-Adolescent,
pubmed-meshheading:14566967-Adult,
pubmed-meshheading:14566967-Aged,
pubmed-meshheading:14566967-Antigens, CD95,
pubmed-meshheading:14566967-Apoptosis,
pubmed-meshheading:14566967-Arthritis, Rheumatoid,
pubmed-meshheading:14566967-Caspase 3,
pubmed-meshheading:14566967-Caspases,
pubmed-meshheading:14566967-Cells, Cultured,
pubmed-meshheading:14566967-Chondrocytes,
pubmed-meshheading:14566967-Enzyme Inhibitors,
pubmed-meshheading:14566967-Free Radical Scavengers,
pubmed-meshheading:14566967-Humans,
pubmed-meshheading:14566967-Interleukin-1,
pubmed-meshheading:14566967-Middle Aged,
pubmed-meshheading:14566967-Mitogen-Activated Protein Kinases,
pubmed-meshheading:14566967-Nitric Oxide,
pubmed-meshheading:14566967-Nitric Oxide Donors,
pubmed-meshheading:14566967-Osteoarthritis,
pubmed-meshheading:14566967-Proteins,
pubmed-meshheading:14566967-Reactive Oxygen Species,
pubmed-meshheading:14566967-omega-N-Methylarginine,
pubmed-meshheading:14566967-p38 Mitogen-Activated Protein Kinases
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pubmed:year |
2003
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pubmed:articleTitle |
Role of nitric oxide, reactive oxygen species, and p38 MAP kinase in the regulation of human chondrocyte apoptosis.
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pubmed:affiliation |
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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