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Provedor de dados:  BJMBR
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
Direitos:  info:eu-repo/semantics/openAccess
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