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Int Immunopharmacol ; 3(9): 1273-80, 2003 Sep.
Article in English | MEDLINE | ID: mdl-12890425

ABSTRACT

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.


Subject(s)
Fibroblasts/drug effects , Interferon-gamma/pharmacology , Myoblasts/cytology , Actins/biosynthesis , Actins/genetics , Actins/physiology , Cell Differentiation/drug effects , Cell Line/drug effects , Cell Line/metabolism , Dupuytren Contracture/etiology , Fibroblasts/cytology , Fibroblasts/metabolism , Gene Expression Regulation/drug effects , Humans , RNA, Messenger/biosynthesis , Transforming Growth Factor beta/pharmacology , Transforming Growth Factor beta1
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