Matches in SemOpenAlex for { <https://semopenalex.org/work/W2011446543> ?p ?o ?g. }
- W2011446543 endingPage "1528" @default.
- W2011446543 startingPage "1518" @default.
- W2011446543 abstract "An important mechanism contributing to cartilage destruction in arthritis is chondrocyte desensitization toward its main anabolic factor, insulin-like growth factor 1 (IGF-1). In this study, we sought to determine the role of suppressor of cytokine signaling 3 (SOCS-3) in the induction of IGF-1 desensitization of murine chondrocytes.Chondrocyte responsiveness to IGF-1 was assessed by 35S-sulfate incorporation into proteoglycans (PGs), via aggrecan messenger RNA expression, using quantitative real-time polymerase chain reaction or insulin receptor substrate 1 (IRS-1) tyrosine phosphorylation (Western blot analysis). IGF-1 desensitization of patellar chondrocytes was studied in zymosan-induced arthritis. IGF-1 desensitization was induced in patellar cartilage explants or the H4 chondrocyte cell line, exposed to interleukin-1alpha (IL-1alpha). SOCS-3 protein expression was assessed by immunohistochemistry or by Western blot analysis of protein extracts. The role of SOCS-3 in IGF-1 signaling was elucidated by adenoviral overexpression.Exposure of murine articular cartilage to IL-1 caused a significant decrease in IGF-1-induced PG synthesis. This effect also occurred in inducible nitric oxide synthase-knockout mice, revealing the involvement of a secondary IL-1-induced factor other than nitric oxide. We showed that IL-1 significantly up-regulated SOCS-3 transcription and protein synthesis in H4 chondrocytes. In contrast, IL-18 was unable to induce SOCS-3 expression and failed to induce chondrocyte IGF-1 desensitization. Histologic analysis of samples from arthritic knee joints revealed high expression of SOCS-3 in chondrocytes. Through adenoviral overexpression of SOCS-3, we obtained direct evidence that SOCS-3 inhibits IGF-1-mediated cell signaling, since IRS-1 phosphorylation was reduced.This study demonstrates that IL-1-induced SOCS-3 expression is a novel mechanism of IGF-1 desensitization in chondrocytes; in conjunction with nitric oxide it can contribute to cartilage damage during arthritis." @default.
- W2011446543 created "2016-06-24" @default.
- W2011446543 creator A5023426980 @default.
- W2011446543 creator A5036752858 @default.
- W2011446543 creator A5045199963 @default.
- W2011446543 creator A5049232513 @default.
- W2011446543 creator A5054720495 @default.
- W2011446543 creator A5070431178 @default.
- W2011446543 creator A5076729726 @default.
- W2011446543 date "2006-04-27" @default.
- W2011446543 modified "2023-10-16" @default.
- W2011446543 title "A novel role for suppressor of cytokine signaling 3 in cartilage destruction via induction of chondrocyte desensitization toward insulin-like growth factor" @default.
- W2011446543 cites W123183995 @default.
- W2011446543 cites W1510351486 @default.
- W2011446543 cites W1544116994 @default.
- W2011446543 cites W1899997617 @default.
- W2011446543 cites W1995111560 @default.
- W2011446543 cites W1995246567 @default.
- W2011446543 cites W1998060649 @default.
- W2011446543 cites W2021086063 @default.
- W2011446543 cites W2023623228 @default.
- W2011446543 cites W2032443713 @default.
- W2011446543 cites W2039214874 @default.
- W2011446543 cites W2042469661 @default.
- W2011446543 cites W2050720508 @default.
- W2011446543 cites W2050959488 @default.
- W2011446543 cites W2053865268 @default.
- W2011446543 cites W2055478328 @default.
- W2011446543 cites W2060808005 @default.
- W2011446543 cites W2068198693 @default.
- W2011446543 cites W2071367062 @default.
- W2011446543 cites W2085580043 @default.
- W2011446543 cites W2112262032 @default.
- W2011446543 cites W2115237069 @default.
- W2011446543 cites W2117382612 @default.
- W2011446543 cites W2119596771 @default.
- W2011446543 cites W2121672863 @default.
- W2011446543 cites W2132684361 @default.
- W2011446543 cites W2140793658 @default.
- W2011446543 cites W2143971425 @default.
- W2011446543 cites W2146272458 @default.
- W2011446543 cites W2148531175 @default.
- W2011446543 cites W2155493931 @default.
- W2011446543 cites W2155597119 @default.
- W2011446543 cites W2414476989 @default.
- W2011446543 cites W4294216491 @default.
- W2011446543 cites W4322703114 @default.
- W2011446543 doi "https://doi.org/10.1002/art.21752" @default.
- W2011446543 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16646036" @default.
- W2011446543 hasPublicationYear "2006" @default.
- W2011446543 type Work @default.
- W2011446543 sameAs 2011446543 @default.
- W2011446543 citedByCount "47" @default.
- W2011446543 countsByYear W20114465432012 @default.
- W2011446543 countsByYear W20114465432013 @default.
- W2011446543 countsByYear W20114465432014 @default.
- W2011446543 countsByYear W20114465432015 @default.
- W2011446543 countsByYear W20114465432016 @default.
- W2011446543 countsByYear W20114465432017 @default.
- W2011446543 countsByYear W20114465432020 @default.
- W2011446543 countsByYear W20114465432021 @default.
- W2011446543 countsByYear W20114465432023 @default.
- W2011446543 crossrefType "journal-article" @default.
- W2011446543 hasAuthorship W2011446543A5023426980 @default.
- W2011446543 hasAuthorship W2011446543A5036752858 @default.
- W2011446543 hasAuthorship W2011446543A5045199963 @default.
- W2011446543 hasAuthorship W2011446543A5049232513 @default.
- W2011446543 hasAuthorship W2011446543A5054720495 @default.
- W2011446543 hasAuthorship W2011446543A5070431178 @default.
- W2011446543 hasAuthorship W2011446543A5076729726 @default.
- W2011446543 hasConcept C104317684 @default.
- W2011446543 hasConcept C105702510 @default.
- W2011446543 hasConcept C126322002 @default.
- W2011446543 hasConcept C134018914 @default.
- W2011446543 hasConcept C142724271 @default.
- W2011446543 hasConcept C153911025 @default.
- W2011446543 hasConcept C170493617 @default.
- W2011446543 hasConcept C185592680 @default.
- W2011446543 hasConcept C197534660 @default.
- W2011446543 hasConcept C204787440 @default.
- W2011446543 hasConcept C2775960820 @default.
- W2011446543 hasConcept C2776164576 @default.
- W2011446543 hasConcept C2776415932 @default.
- W2011446543 hasConcept C2778690821 @default.
- W2011446543 hasConcept C2780550940 @default.
- W2011446543 hasConcept C2780689927 @default.
- W2011446543 hasConcept C2781403057 @default.
- W2011446543 hasConcept C3020332539 @default.
- W2011446543 hasConcept C502942594 @default.
- W2011446543 hasConcept C55493867 @default.
- W2011446543 hasConcept C71924100 @default.
- W2011446543 hasConcept C86803240 @default.
- W2011446543 hasConcept C95444343 @default.
- W2011446543 hasConceptScore W2011446543C104317684 @default.
- W2011446543 hasConceptScore W2011446543C105702510 @default.
- W2011446543 hasConceptScore W2011446543C126322002 @default.
- W2011446543 hasConceptScore W2011446543C134018914 @default.
- W2011446543 hasConceptScore W2011446543C142724271 @default.