摘要
Macrophage migration inhibitory factor tory processes,and inflammation is known to play an （MIF） is a pleiotropic cytokine that controls inflamma 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.
Macrophage migration inhibitory factor tory processes,and inflammation is known to play an （MIF） is a pleiotropic cytokine that controls inflamma 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.
基金
supported by National Natural Science Foundation of China(No.81000084)
China Postdoctoral Science Foundation(No.20100470894)
Medical Scientific Research Foundation of Guangdong Province(No.B2010014)
