© 2003 by European Society of Cardiology
Copyright © 2003, European Society of Cardiology
Mac-1 and Fas activities are concurrently required for execution of smooth muscle cell death by M-CSF-stimulated macrophages
aDivision of Cardiology, Department of Medicine, Duke University Medical Center, Box 3845, Durham, NC 27700, USA
bDivision of Cardiology, Emory University, Atlanta, GA, USA
cDorothy M. Davis Heart and Lung Institute, Ohio State University, Columbus, OH, USA
dThe Lindner Research Center/Ohio Heart Health Center, Cincinnati, OH, USA
golds017{at}mc.duke.edu
* Corresponding author. Tel.: +1-919-668-1755; fax: +1-919-668-1861.
Objective: We have previously shown that macrophage colony stimulating factor (M-CSF), a potent survival and mitogenic factor for monocytes/macrophages (MM), enables MM to induce vascular smooth muscle cell (VSMC) apoptosis. The killing requires the binding of MM to VSMC via Mac-1 (CD11b/CD18) on MM and intracellular adhesion molecule-1 (ICAM-1) on VSMC. We hypothesized that, in addition to Mac-1 binding, the killing process requires the activation of the Fas–death receptor pathway, which can be blocked at the level of Fas–Fas ligand interaction. Methods and Results: Human peripheral blood monocytes and VSMC were isolated and cultured as previously described. Soluble Fas (sFas) was overexpressed in VSMC by transduction using adenovirus specifying soluble Fas (Ad3hsFas). M-CSF markedly increased the expression of ICAM-1 in VSMC, resulting in enhanced clustering of MM on the surface of VSMC (
3 MM per VSMC). MM, but not VSMC, expressed Fas-ligand (FasL), and VSMC apoptosis was inhibited by secretion of sFas by VSMC upon Ad3sFas transduction. Conclusions: MM and M-CSF-induced VSMC killing requires MM binding to VSMC mediated by Mac-1 and ICAM-1, and Fas–FasL interaction.
KEYWORDS Apoptosis; Smooth muscle; Infection/inflammation; Macrophages; Growth factors
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