Macrophage migration inhibitory factor as a redox-sensitive cytokine in cardiac myocytes

Abstract

Objective: Macrophage migration inhibitory factor (MIF), which plays a pivotal role in the control of inflammatory responses, was first characterized as a T-cell cytokine, but later was also found as a pituitary peptide released in response to infection and stress. However, MIF's role and expression in the myocardium has never been reported. The goal of this study is to examine MIF in the myocardium. Methods and results: MIF protein and mRNA levels were assayed using enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Increased MIF concentrations were detected in the sera of patients with acute myocardial infarction (AMI). In cultured rat cardiac myocytes, significant amounts of MIF were produced in response to hypoxia and hydrogen peroxide (H O ), but not to angiotensin II, endothelin-1, interleukin-1b (IL-1b) or tumor necrosis factor a (TNFa). 2 2 H O -induced MIF production increased in a time-and dose-dependent manner and was completely abolished in the presence of catalase.