Chondrocyte phenotype and cell survival are regulated by culture conditions and by specific cytokines through the expression of Sox-9 transcription factor

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dc.contributor.authorKolettas, E.en
dc.contributor.authorMuir, H. I.en
dc.contributor.authorBarrett, J. C.en
dc.contributor.authorHardingham, T. E.en
dc.date.accessioned2015-11-24T19:30:40Z
dc.date.available2015-11-24T19:30:40Z
dc.identifier.issn1462-0324-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/23146
dc.rightsDefault Licence-
dc.subjectAggrecansen
dc.subjectAnimalsen
dc.subjectAntimetabolites, Antineoplastic/pharmacologyen
dc.subjectApoptosis/drug effects/immunologyen
dc.subjectAzacitidine/pharmacologyen
dc.subjectBiglycanen
dc.subjectCell Line, Transformeden
dc.subjectCell Survival/immunologyen
dc.subjectChondrocytes/*cytology/*immunologyen
dc.subjectCollagen Type II/geneticsen
dc.subjectCollagen Type IX/geneticsen
dc.subjectCricetinaeen
dc.subject*Extracellular Matrix Proteinsen
dc.subjectFetus/cytologyen
dc.subjectGene Expression/drug effects/immunologyen
dc.subjectHigh Mobility Group Proteins/*genetics/immunologyen
dc.subjectInsulin-Like Growth Factor I/*pharmacologyen
dc.subjectInterleukin-1/*pharmacologyen
dc.subjectLectins, C-Typeen
dc.subjectMesocricetusen
dc.subjectPhenotypeen
dc.subjectProteins/geneticsen
dc.subjectProteoglycans/geneticsen
dc.subjectRNA, Messenger/analysisen
dc.subjectSOX9 Transcription Factoren
dc.subjectTranscription Factors/*genetics/immunologyen
dc.titleChondrocyte phenotype and cell survival are regulated by culture conditions and by specific cytokines through the expression of Sox-9 transcription factoren
heal.abstractOBJECTIVE: To investigate the effects of culture conditions, serum and specific cytokines such as insulin-like growth factor (IGF) 1 and interleukin (IL) 1alpha on phenotype and cell survival in cultures of Syrian hamster embryonic chondrocyte-like cells (DES4(+).2). METHODS: Proteins and RNA extracted from subconfluent and confluent early- and late-passage DES4(+).2 cells cultured in the presence or absence of serum and IL-1alpha or IGF-1 or both cytokines together were analysed for the expression of chondrocyte-specific genes and for the chondrogenic transcription factor Sox-9 by Western and Northern blotting. Apoptosis was assessed by agarose gel electrophoresis of labelled low-molecular weight DNA extracted from DES4(+).2 cells and another Syrian hamster embryonic chondrocyte-like cell line, 10W(+).1, cultured under the different conditions and treatments. RESULTS: Early passage DES4(+).2 cells expressed chondrocyte-specific molecules such as collagen types alpha1(II) and alpha1(IX), aggrecan, biglycan and link protein and collagen types alpha1(I) and alpha1(X) mRNAs, suggesting a prehypertrophic chondrocyte-like phenotype. The expression of all genes investigated was cell density- and serum-dependent and was low to undetectable in cell populations from later passages. Early-passage DES4(+).2 and 10W(+).1 cells survived when cultured at low cell density, but died by apoptosis when cultured at high cell density in the absence of serum or IGF-1. IGF-1 and IL-1alpha had opposite and antagonistic effects on the chondrocyte phenotype and survival. Whereas IL-1alpha acting alone suppressed cartilage-specific gene expression without significantly affecting cell survival, IGF-1 increased the steady-state mRNA levels and relieved the IL-1alpha-induced suppression of all the chondrocyte-specific genes investigated; it also enhanced chondrocyte survival. Suppression of the chondrocyte phenotype by the inflammatory cytokine IL-1alpha correlated with marked down-regulation of the transcription factor Sox-9, which was relieved by IGF-1. The expression of the Sox9 gene was closely correlated with the expression of the chondrocyte-specific genes under all conditions and treatments. CONCLUSIONS: The results suggest that the effects of cartilage anabolic and catabolic cytokines IGF-1 and IL-1alpha on the expression of the chondrocyte phenotype are mediated by Sox-9. As Sox-9 appears to be essential for matrix production, the potent effect of IL-1alpha in suppressing Sox-9 expression may limit the ability of cartilage to repair during inflammatory joint diseases.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11600745-
heal.identifier.secondaryhttp://rheumatology.oxfordjournals.org/content/40/10/1146.full.pdf-
heal.journalNameRheumatology (Oxford)en
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2001-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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