| pubmed-article:14566967 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14566967 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:14566967 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:14566967 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:14566967 | lifeskim:mentions | umls-concept:C0225369 | lld:lifeskim |
| pubmed-article:14566967 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:14566967 | lifeskim:mentions | umls-concept:C0162772 | lld:lifeskim |
| pubmed-article:14566967 | lifeskim:mentions | umls-concept:C1120843 | lld:lifeskim |
| pubmed-article:14566967 | lifeskim:mentions | umls-concept:C1366876 | lld:lifeskim |
| pubmed-article:14566967 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:14566967 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:14566967 | pubmed:dateCreated | 2003-10-20 | lld:pubmed |
| pubmed-article:14566967 | 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. | lld:pubmed |
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| pubmed-article:14566967 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14566967 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14566967 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:14566967 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14566967 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:14566967 | pubmed:issn | 0021-9541 | lld:pubmed |
| pubmed-article:14566967 | pubmed:author | pubmed-author:LotzMartinM | lld:pubmed |
| pubmed-article:14566967 | pubmed:author | pubmed-author:KühnKlausK | lld:pubmed |
| pubmed-article:14566967 | pubmed:author | pubmed-author:ShikhmanAlexa... | lld:pubmed |
| pubmed-article:14566967 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14566967 | pubmed:volume | 197 | lld:pubmed |
| pubmed-article:14566967 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14566967 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14566967 | pubmed:pagination | 379-87 | lld:pubmed |
| pubmed-article:14566967 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:14566967 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:14566967 | pubmed:articleTitle | Role of nitric oxide, reactive oxygen species, and p38 MAP kinase in the regulation of human chondrocyte apoptosis. | lld:pubmed |
| pubmed-article:14566967 | pubmed:affiliation | Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA. | lld:pubmed |
| pubmed-article:14566967 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14566967 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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