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Background Macrophage migration inhibitory factor(MIF)is a pleiotropic cytokine that controls inflammatory processes,and inflammation is known to play an important role in the pathogenesis of atrial fibrillation(AF).The present study sought to investigate whether MIF played an important role in the pathogenesis of AF.Methods MIF protein and mRNA levels in specimens of human right atrial appendage(from patients with AF or sinus rhythm)or atrium myocytes(HL-1 cells)were assayed using enzyme-linked immunosorbent assay(ELISA),real time PCR and Western blot,respectively.Results MIF expression levels were increased in AF when compared to SR.In cultured HL-1 cells,significant amounts of MIF were produced in response to hydrogen peroxide(H2O2).H2O2-induced MIF production increased in a dose-dependent manner and was completely abolished in the presence of catalase.The H2O2-induced MIF production was completely inhibited by tyrosine kinase inhibitor genistein and PP1.Conclusions These results implicate MIF might be involved in the pathogensis of AF as a redox-sensitive cytokine.[S Chin J Cardiol 2011;12(3):178-186]
Background Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that controls inflammatory processes, and inflammation is known to play an important role in the pathogenesis of atrial fibrillation (AF). The present study sought to investigate whether MIF played an important role in the pathogenesis of AF. Methods MIF protein and mRNA levels in specimens of human right atrial appendage (from patients with AF or sinus rhythm) or atrium myocytes (HL-1 cells) were assayed using enzyme-linked immunosorbent assay (ELISA) and Western blot, respectively. Results MIF expression levels were increased in AF when compared to SR. cultured HL-1 cells, significant amounts of MIF were produced in response to hydrogen peroxide (H2O2) .H2O2-induced MIF production increased in a dose -dependent manner and was completely abolished in the presence of catalase.The H2O2-induced MIF production was completely inhibited by tyrosine kinase inhibitor genistein and PP1.Conclusions These results im plicate MIF might be involved in the pathogensis of AF as a redox-sensitive cytokine. [S Chin J Cardiol 2011; 12 (3): 178-186]