Human Blood-Derived Macrophages Induce Apoptosis in Human Plaque-Derived Vascular Smooth Muscle Cells by Fas-Ligand/Fas Interactions

Arteriosclerosis, Thrombosis, and Vascular Biology - Tập 21 Số 9 - Trang 1402-1407 - 2001
Joseph J. Boyle1, David E. Bowyer1, Peter L. Weissberg1, Martin R. Bennett1
1From the Unit of Cardiovascular Medicine, Addenbrooke’s Hospital (J.J.B., P.L.W., M.R.B.), and the Department of Pathology, University of Cambridge (D.E.B.), Cambridge, UK.

Tóm tắt

Human atherosclerotic plaques that rupture are characterized by relatively low vascular smooth muscle cell (VSMC) and high inflammatory cell contents. Ruptured plaques also contain higher numbers of apoptotic VSMCs than do stable lesions, suggesting that VSMC apoptosis may promote plaque rupture. We examined the ability of human monocytes/macrophages to induce apoptosis of VSMCs derived from human carotid plaque, aortic media, and coronary media. Macrophages, but not T lymphocytes, induced a dose-dependent apoptosis of VSMCs, which required monocyte maturation to macrophages and direct cell-cell contact/proximity. VSMC apoptosis was inhibited by neutralizing antibodies to Fas-ligand (Fas-L) or an Fas-Fc fusion protein, indicating the requirement for membrane-bound Fas and Fas-L. Monocyte maturation was associated with increased surface expression of Fas-L, coincident with the onset of cytotoxicity. VSMCs expressed surface Fas, which was increased in plaque VSMCs, and plaque VSMCs also underwent Fas-induced apoptosis. We conclude that human macrophages potently induce human VSMC apoptosis, which requires direct cell-cell interactions and is in part dependent on Fas/Fas-L interactions. Macrophage-induced VSMC apoptosis may therefore directly promote plaque rupture.

Từ khóa


Tài liệu tham khảo

10.1056/NEJM199901143400207

10.1136/hrt.69.5.377

10.1161/circ.92.3.657

Rekhter MD, Zhang K, Narayanan AS, Phan S, Schork MA, Gordon D. Type I collagen gene expression in human atherosclerosis: localization to specific plaque regions. Am J Pathol. . 1993; 143: 1634–1648.

10.1016/S0008-6363(98)00286-7

10.1172/JCI117917

10.1038/bjc.1972.33

10.1016/S0092-8674(00)81874-7

Bjorkerud S, Bjorkerud B. Apoptosis is abundant in human atherosclerotic lesions, especially in inflammatory cells (macrophages and T cells), and may contribute to the accumulation of gruel and plaque instability. Am J Pathol. . 1996; 149: 367–380.

Geng YJ, Libby P. Evidence for apoptosis in advanced human atheroma: colocalization with interleukin-1 β-converting enzyme. Am J Pathol. . 1995; 147: 251–266.

10.1016/S0008-6363(98)00318-6

10.1161/atvb.16.1.19

10.1161/atvb.17.10.2200

10.4049/jimmunol.159.4.1594

10.1172/JCI115718

10.1016/0022-1759(86)90415-1

10.1161/res.81.4.591

10.1161/res.82.6.704

10.1126/science.282.5387.290

Lopez CA, Holmes DR, Liao S, Scott MJ, Wickline SA, Thompson RW. Decreased vascular smooth muscle cell density in medial degeneration of human abdominal aortic aneurysms. Am J Pathol. . 1997; 150: 993–1007.

10.1042/bj3150021

10.1073/pnas.92.17.7804

10.4049/jimmunol.150.8.3478

10.1016/0092-8674(93)80047-I

10.1182/blood.V89.6.1931

10.1016/S0955-0674(99)80034-9

10.1038/nm0198-031

10.1002/j.1460-2075.1995.tb07096.x

10.1084/jem.185.8.1511

10.1084/jem.190.11.1679