| Posttranscriptional effect of insulin-like growth factor-I on interleukin-1beta-induced type II-secreted phospholipase A2 gene expression in rabbit articular chondrocytes. | |
MedLine Citation:
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PMID: 9109430 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Large amounts of type II-secreted phospholipase A2 (type II sPLA2) are secreted into inflammatory synovial fluid and they are believed to induce the synthesis of lipid mediators by articular chondrocytes. Preliminary experiments showed that insulin-like growth factor-I, which counteracts cartilage degradation in arthritis, inhibits interleukin-1beta-induced type II sPLA2 gene expression in rabbit articular chondrocytes (Berenbaum, F., G. Thomas, S. Poiraudeau, G. Bereziat, M.T. Corvol, and J. Masliah. 1994. FEBS Lett. 340: 51-55). The present study showed that IL-1beta induced the sustained synthesis of prostaglandin E2 and a parallel increase in type II sPLA2 gene expression (assessed by enzymatic activity and Northern blot analysis), but no increase in cytosolic PLA2 gene expression (assessed by Northern and Western blot analysis) or cytosolic PLA2 activity in rabbit articular chondrocytes. IGF-I inhibited both IL-1beta-stimulated PGE2 synthesis and type II sPLA2 gene expression, but had no effect on cytosolic PLA2 gene expression. Nuclear run-on experiments revealed that IL-1beta stimulated the transcription rate of type II sPLA2 gene, giving rise to long-lived mRNA in cells treated with actinomycin D. IGF-I did not affect transcription rate, suggesting that it acts as a post-transcriptional step. Sucrose density gradient analysis of the translation step showed no effect of IGF-I on the entry of type II sPLA2 mRNA into the polysomal pool or on its distribution into the various polysomal complexes, suggesting that IGF-I does not act on the translation of the mRNA. Lastly, IGF-I strongly decreased the half-life of IL-1beta-induced type II sPLA2 mRNA (from 92 to 12 h), suggesting that IGF-I destabilizes mRNA. These data demonstrate that IL-1beta stimulates the transcription rate of the type II sPLA2 gene and gives rise to a very stable mRNA. In contrast, IGF-I decreases the half-life of the type II sPLA2 message. |
Authors:
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C Jacques; G Béréziat; L Humbert; J L Olivier; M T Corvol; J Masliah; F Berenbaum |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of clinical investigation Volume: 99 ISSN: 0021-9738 ISO Abbreviation: J. Clin. Invest. Publication Date: 1997 Apr |
Date Detail:
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Created Date: 1997-05-09 Completed Date: 1997-05-09 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 7802877 Medline TA: J Clin Invest Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1864-72 Citation Subset: AIM; IM |
Affiliation:
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Biochemistry and Molecular Biology Laboratory, Faculty of Medicine of St. Antoine, University Pierre and Marie Curie, Paris, France. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amino Acid Sequence Animals Base Sequence Cartilage, Articular / cytology, drug effects*, metabolism* Cells, Cultured DNA, Complementary / genetics Dinoprostone / biosynthesis Gene Expression Regulation, Enzymologic / drug effects Humans Insulin-Like Growth Factor I / pharmacology* Interleukin-1 / pharmacology* Kinetics Molecular Sequence Data Phospholipases A / classification, genetics*, metabolism Phospholipases A2 RNA, Messenger / genetics, metabolism Rabbits Recombinant Proteins / pharmacology Ribosomes / drug effects, metabolism Sequence Homology, Amino Acid |
| Chemical | |
Reg. No./Substance:
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0/DNA, Complementary; 0/Interleukin-1; 0/RNA, Messenger; 0/Recombinant Proteins; 363-24-6/Dinoprostone; 67763-96-6/Insulin-Like Growth Factor I; EC 3.1.1.-/Phospholipases A; EC 3.1.1.4/Phospholipases A2 |
| Comments/Corrections | |
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