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Titolo:
Chondrocyte phenotype and cell survival are regulated by culture conditions and by specific cytokines through the expression of Sox-9 transcription factor
Autore:
Kolettas, E; Muir, HI; Barrett, JC; Hardingham, TE;
Indirizzi:
Univ Manchester, Sch Biol Sci, Wellcome Trust Ctr Cell Matrix Res, Manchester M13 9PT, Lancs, England Univ Manchester Manchester Lancs England M13 9PT M13 9PT, Lancs, England NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA NIEHS Res Triangle Pk NC USA 27709 ab, NIH, Res Triangle Pk, NC 27709 USA
Titolo Testata:
RHEUMATOLOGY
fascicolo: 10, volume: 40, anno: 2001,
pagine: 1146 - 1156
SICI:
1462-0324(200110)40:10<1146:CPACSA>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
II COLLAGEN GENE; HUMAN ARTICULAR-CARTILAGE; SRY-RELATED GENE; AUTOSOMAL SEX REVERSAL; TUMOR-SUPPRESSOR GENE; HAMSTER EMBRYO CELLS; GROWTH FACTOR-I; NEOPLASTIC PROGRESSION; CAMPOMELIC DYSPLASIA; MESSENGER-RNAS;
Keywords:
chondrocytes; gene expression; cytokines; apoptosis; Sox9;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
74
Recensione:
Indirizzi per estratti:
Indirizzo: Kolettas, E Univ Ioannina, Sch Med, Physiol Lab, Cell & Mol Physiol Unit, GR-45110 Ioannina, Greece Univ Ioannina Ioannina Greece GR-45110 5110 Ioannina, Greece
Citazione:
E. Kolettas et al., "Chondrocyte phenotype and cell survival are regulated by culture conditions and by specific cytokines through the expression of Sox-9 transcription factor", RHEUMATOLOG, 40(10), 2001, pp. 1146-1156

Abstract

Objective. To investigate the effects of culture conditions, serum and specific cytokines such as insulin-like growth factor (IGF) 1 and interleukin (IL) 1 alpha 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-1 alpha 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 get 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-1 alpha had opposite and antagonistic effects on the chondrocyte phenotype and survival. Whereas LL-lot acting alone suppressed cartilage-specific gene expression without significantly affecting cell survival, IGF-1 increased the steady-state mRNA levels and relieved the IL-1 alpha -induced suppression of all the chondrocyte-specific genes investigated, it also enhanced chondrocyte survival. Suppression of the chondrocyte phenotype by the inflammatory cytokine IL-1 alpha 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-1 alpha 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-1 alpha in suppressing Sox-9 expression may limit the ability of cartilage to repair during inflammatory joint diseases.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 07:12:54