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Am J Physiol Heart Circ Physiol 288: H293-H301, 2005. First published September 9, 2004; doi:10.1152/ajpheart.00165.2004
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TNF-{alpha} induces proliferation or apoptosis in human saphenous vein smooth muscle cells depending on phenotype

Zhongbiao Wang,1 Pulipaka J. Rao,2 Manuel R. Castresana,3 and Walter H. Newman1,3,4

1Division of Basic Medical Science, and Departments of 2Psychiatry and Behavioral Science, 3Anesthesiology, and 4Surgery, Mercer University School of Medicine, and Medical Center of Central Georgia, Macon, Georgia

Submitted 17 February 2004 ; accepted in final form 1 September 2004

Tumor necrosis factor (TNF)-{alpha} is implicated in development of restenotic and atherosclerotic vascular lesions, which are pathological processes involving both proliferation and apoptosis of vascular smooth muscle cells (VSMCs). Human VSMCs were recently found to contain heterogeneous subpopulations. We therefore examined whether TNF has different effects on distinct subpopulations of VSMCs. With the use of cloning techniques, two stable subpopulations of VSMCs were isolated from human saphenous vein: spindle- and epithelioid-shaped smooth muscle cells (Sp- and Ep-SMCs, respectively). We found that TNF stimulated growth in Sp-SMCs but had a toxic effect on Ep-SMCs. TNF did not induce apoptosis in Sp-SMCs as determined by nuclear staining and cellular DNA electrophoresis. In contrast, the reduction of viability in Ep-SMCs was associated with induction of apoptosis as characterized by cellular DNA fragmentation and nuclear condensation. Higher levels of the TNF-R1 receptor subtype were detected in membrane preparations from Ep-SMCs than in membranes from Sp-SMCs. Activation of caspase-3 was also selectively induced in Ep-SMCs but not in Sp-SMCs. Cycloheximide, an inhibitor of protein synthesis, enhanced the toxicity of TNF in Ep-SMCs. This effect of cycloheximide was not seen in Sp-SMCs. The data presented here demonstrate for the first time that TNF either promotes growth or induces apoptosis in human VSMCs depending on phenotype.

tumor necrosis factor-{alpha}; spindle; epithelioid; cycloheximide; atherosclerosis; stenosis


Address for reprint requests and other correspondence: Z. Wang, Division of Basic Medical Science, Mercer Univ. School of Medicine, 1550 College St., Macon, GA 31207 (E-mail: wang_z{at}mercer.edu)




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