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Up-regulation of type II collagen gene by 17 beta-estradiol in articular chondrocytes involves Sp1/3, Sox-9, and estrogen receptor alpha

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Titre :	Up-regulation of type II collagen gene by 17 beta-estradiol in articular chondrocytes involves Sp1/3, Sox-9, and estrogen receptor alpha (2014)
Auteurs :	L. Maneix ; A. Servent ; B. Poree ; D. Ollitrault ; T. Branly ; N. Bigot ; N. Boujrad ; G. Flouriot ; M. Demoor ; K. Boumediene ; S. Moslemi ; P. Galera
Type de document :	Article : texte imprimé
Dans :	J MOL MED (92, 2014-08-02)
Article en page(s) :	p.1179-1200
Langues:	Anglais
Mots-clés :	Mots-clés cheval OESTROGENE ; OSTEOARTHRITE Equivoc Cartilage ; Médecine Humaine
Résumé :	The existence of a link between estrogen deprivation and osteoarthritis (OA) in postmenopausal women suggests that 17?-estradiol (17?-E2) may be a modulator of cartilage homeostasis. Here, we demonstrate that 17?-E2 stimulates, via its receptor human estrogen receptor ? 66 (hER?66), type II collagen expression in differentiated and dedifferentiated (reflecting the OA phenotype) articular chondrocytes. Transactivation of type II collagen gene (COL2A1) by ligand-independent transactivation domain (AF-1) of hER?66 was mediated by \223GC\224 binding sites of the ?266/ ?63-bp promoter, through physical interactions between ER?, Sp1/Sp3, Sox9, and p300, as demonstrated in chromatin immunoprecipitation (ChIP) and Re-Chromatin Immuno- Precipi tation (Re-ChIP) assays in primary and dedifferentiated cells. 17?-E2 and hER?66 increased the DNA-binding activities of Sp1/Sp3 and Sox-9 to both COL2A1 promoter and enhancer regions. Besides, Sp1, Sp3, and Sox-9 small interfering RNAs (siRNAs) prevented hER?66-induced transactivation of COL2A1, suggesting that these factors and their respective cis-regions are required for hER?66-mediated COL2A1 up-regulation. Our results highlight the genomic pathway by which 17?-E2 and hER?66 modulate Sp1/Sp3 heteromer binding activity and simultaneously participate in the recruitment of the essential factors Sox-9 and p300 involved respectively in the chondrocyte-differentiated status and COL2A1 transcriptional activation. These novel findings could therefore be attractive for tissue engineering of cartilage in OA, by the fact that 17?- E2 could promote chondrocyte redifferentiation.
Cote du document numérique :	17356
Classement cheval :	A17

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