Letter to the Editor
De Novo Expression of Macrophage Migration Inhibitory Factor in Atherogenesis
To the Editor:
We read with great interest the article by Lin et al1 on the expression of macrophage migration inhibitory factor (MIF) in atherosclerotic lesions of a hypercholesterolemic rabbit model. They demonstrated, in the early stages of atherogenesis, marked upregulation of MIF mRNA. The protein was detected in vascular endothelial cells with CD68-positive macrophages adhering to endothelial cells and subsequently migrating into the subendothelial space. However, MIF expression by smooth muscle cells was transient during atherogenesis. Interestingly, the accumulation of macrophages was exclusively localized to areas of strong MIF expression, which may be responsible for the development of foam cell–rich lesions in hypercholesterolemic rabbits.
We previously reported that MIF was expressed in macrophages2 and endothelial cells.3 Furthermore, we recently investigated MIF expression in human atherectomy samples obtained from coronary and femoral arteries of patients with coronary and peripheral artery diseases. Strong MIF expression was localized in CD68-positive macrophages, whereas weak MIF expression was detected in α-actin–positive smooth muscle cells of atherosclerotic lesions. These findings suggest that, as observed in a rabbit model by Lin et al,1 macrophages are a major source of MIF expression in human atherosclerotic vessels, and upregulation of MIF expression by these cells may contribute to local macrophage accumulation, ultimately resulting in macrophage-rich atherosclerotic lesion formation in humans.
- © 2001 American Heart Association, Inc.