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Int Immunopharmacol ; 3(9): 1273-80, 2003 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-12890425

RESUMO

Interferon gamma (IFNgamma) has been reported as a possible therapeutic agent for contractile diseases in clinical trials and in vitro studies. It is not yet clear, however, whether IFNgamma simply inhibits myofibroblast generation or downregulates alpha smooth muscle actin (alphaSMA) production in myofibroblasts. In this study, we attempted to clarify how IFNgamma acts in the generation of myofibroblasts, and the production of alphaSMA by myofibroblasts, using immunofluorescence staining, cell capture enzyme immunoassay (CC-EIA) and the reverse transcription polymerase chain reaction (RT-PCR) for alphaSMA. We examined whether IFNgamma could block the TGFbeta1-promoted changes in myofibroblasts or the generation of myofibroblasts by TGFbeta1. IFNgamma strongly blocked the generation of myofibroblasts and moderately inhibited the production of alphaSMA in TGFbeta1-promoted myofibrobasts. These findings indicate that IFNgamma may be effective in the early stage of contractile diseases to prevent the progression of contractile lesions.


Assuntos
Fibroblastos/efeitos dos fármacos , Interferon gama/farmacologia , Mioblastos/citologia , Actinas/biossíntese , Actinas/genética , Actinas/fisiologia , Diferenciação Celular/efeitos dos fármacos , Linhagem Celular/efeitos dos fármacos , Linhagem Celular/metabolismo , Contratura de Dupuytren/etiologia , Fibroblastos/citologia , Fibroblastos/metabolismo , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , RNA Mensageiro/biossíntese , Fator de Crescimento Transformador beta/farmacologia , Fator de Crescimento Transformador beta1
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