Data/hora: 09/06/2024 10:43:20

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