| Registro completo |
| Provedor de dados: |
BJMBR
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| País: |
Brazil
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| Título: |
Involvement of Src tyrosine kinase and protein kinase C in the expression of macrophage migration inhibitory factor induced by H2O2 in HL-1 mouse cardiac muscle cells
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| Autores: |
Rao,F.
Deng,C.Y.
Zhang,Q.H.
Xue,Y.M.
Xiao,D.Z.
Kuang,S.J.
Lin,Q.X.
Shan,Z.X.
Liu,X.Y.
Zhu,J.N.
Yu,X.Y.
Wu,S.L.
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| Data: |
2013-09-01
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| Ano: |
2013
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| Palavras-chave: |
Macrophage migration inhibitory factor
HL-1 cells
Hydrogen peroxide
Atrial fibrillation
Protein kinases
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| Resumo: |
Macrophage migration inhibitory factor (MIF), a pleiotropic cytokine, plays an important role in the pathogenesis of atrial fibrillation; however, the upstream regulation of MIF in atrial myocytes remains unclear. In the present study, we investigated whether and how MIF is regulated in response to the renin-angiotensin system and oxidative stress in atrium myocytes (HL-1 cells). MIF protein and mRNA levels in HL-1 cells were assayed using immunofluorescence, real-time PCR, and Western blot. The result indicated that MIF was expressed in the cytoplasm of HL-1 cells. Hydrogen peroxide (H2O2), but not angiotensin II, stimulated MIF expression in HL-1 cells. H2O2-induced MIF protein and gene levels increased in a dose-dependent manner and were completely abolished in the presence of catalase. H2O2-induced MIF production was completely inhibited by tyrosine kinase inhibitors genistein and PP1, as well as by protein kinase C (PKC) inhibitor GF109203X, suggesting that redox-sensitive MIF production is mediated through tyrosine kinase and PKC-dependent mechanisms in HL-1 cells. These results suggest that MIF is upregulated by HL-1 cells in response to redox stress, probably by the activation of Src and PKC.
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| Tipo: |
Info:eu-repo/semantics/article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2013000900746
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| Editor: |
Associação Brasileira de Divulgação Científica
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| Relação: |
10.1590/1414-431X20132936
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| Formato: |
text/html
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| Fonte: |
Brazilian Journal of Medical and Biological Research v.46 n.9 2013
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| Direitos: |
info:eu-repo/semantics/openAccess
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