Data/hora: 10/06/2024 10:14:49

Provedor de dados: | Brazilian Journal of Medical and Biological Research
País: | Brazil
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
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.
Data: | 2013-09-01
Ano: | 2013
Palavras-chave: | Macrophage migration inhibitory factor; HL-1 cells; Hydrogen peroxide; Atrial fibrillation; Protein kinases.
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.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2013000900746
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/1414-431X20132936
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.46 n.9 2013
Fonte: | info:eu-repo/semantics/openAccess