Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/199895
Type: Artigo de periódico
Title: Interferon Beta Modulates Major Histocompatibility Complex Class I (mhc I) And Cd3-zeta Expression In Pc12 Cells.
Author: Inácio, Rodrigo Fabrizzio
Zanon, Renata Graciele
Verinaud, Liana
de Oliveira, Alexandre Leite Rodrigues
Abstract: It has been demonstrated that the major histocompatibility complex of class I (MHC I) up regulation by exogenous treatment with interferon beta (IFNbeta) influences the glial reaction and synaptic elimination process. Therefore, the present study aimed to investigate the effects of IFNbeta treatment on the expression of MHC I, CD3-zeta (a subunit of MHC I receptor) and synaptic formation in PC12 cells, an in vitro model for studying the synaptic formation/elimination process. For this purpose, established cultures were subjected to IFNbeta (500 and 1000IU/ml) treatment for 5, 10 and 15 days. The cells were then fixed and processed for immunocytochemistry with antisera against MHC I (OX18), CD3-zeta and synaptophysin. The results were compared with control cultures only treated with basal medium. IFNbeta (500IU/ml) modulated the MHC I expression in PC12 cells, especially after 10 days of treatment. In this sense, IFNbeta induced MHC I as well as CD3-zeta up regulation. It was observed that the highest dose caused culture degeneration. Interestingly, differential regulation of MHC I was paralleled by enhancement in synaptic network remodeling. Altogether, the present data indicate that PC12 cells may be used as an in vitro model for studying MHC I modulation and synaptic plasticity. It also reinforced the role of IFNbeta on the synaptic elimination process.
Subject: Animals
Antigens, Cd3
Histocompatibility Antigens Class I
Interferon-beta
Pc12 Cells
Rats
Synaptophysin
Up-regulation
Rights: fechado
Identifier DOI: 10.1016/j.neulet.2012.02.046
Address: http://www.ncbi.nlm.nih.gov/pubmed/22387456
Date Issue: 2012
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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