Data/hora: 09/06/2024 11:36:53

Provedor de dados: 	56	
País: 	Brazil	
Título: 	Cotransfected human chondrocytes: over-expression of IGF-I and SOX9 enhances the synthesis of cartilage matrix components collagen-II and glycosaminoglycans	
Autores: 	Simental-Mendía,M.; Lara-Arias,J.; Álvarez-Lozano,E.; Said-Fernández,S.; Soto-Domínguez,A.; Padilla-Rivas,G. R.; Martínez-Rodríguez,H. G.	
Data: 	2015-12-01	
Ano: 	2015	
Palavras-chave: 	Type II collagen; Glycosaminoglycans; IGF-I/SOX9 transgenes; Human chondrocytes; Articular cartilage; Cotransfection.	
Resumo: 	Damage to cartilage causes a loss of type II collagen (Col-II) and glycosaminoglycans (GAG). To restore the original cartilage architecture, cell factors that stimulate Col-II and GAG production are needed. Insulin-like growth factor I (IGF-I) and transcription factor SOX9 are essential for the synthesis of cartilage matrix, chondrocyte proliferation, and phenotype maintenance. We evaluated the combined effect of IGF-I and SOX9 transgene expression on Col-II and GAG production by cultured human articular chondrocytes. Transient transfection and cotransfection were performed using two mammalian expression plasmids (pCMV-SPORT6), one for each transgene. At day 9 post-transfection, the chondrocytes that were over-expressing IGF-I/SOX9 showed 2-fold increased mRNA expression of the Col-II gene, as well as a 57% increase in Col-II protein, whereas type I collagen expression (Col-I) was decreased by 59.3% compared with controls. The production of GAG by these cells increased significantly compared with the controls at day 9 (3.3- vs 1.8-times, an increase of almost 83%). Thus, IGF-I/SOX9 cotransfected chondrocytes may be useful for cell-based articular cartilage therapies.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015001201063	
Editor: 	Associação Brasileira de Divulgação Científica	
Relação: 	10.1590/1414-431x20154732	
Formato: 	text/html	
Fonte: 	Brazilian Journal of Medical and Biological Research  v.48 n.12 2015	
Fonte: 	info:eu-repo/semantics/openAccess