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induces proliferation or apoptosis in human saphenous vein smooth muscle cells depending on phenotype
* To whom correspondence should be addressed. E-mail: wang_z{at}mercer.edu.
Tumor necrosis factor-
(TNF) is implicated in development of restenotic and atherosclerotic vascular lesions, pathological processes involving both proliferation and apoptosis of vascular smooth muscle cells (VSMC). Human VSMC were recently found to contain heterogeneous subpopulations. We therefore examined whether TNF has different effects on distinct subpopulations of VSMC. Using cloning techniques, two stable subpopulations of VSMC were isolated from human saphenous vein: 1) spindle-shaped cells (Sp-SMC) and 2) epitheloid-shaped cells (Ep-SMC). We found that TNF stimulated growth in Sp-SMC but had a toxic effect on Ep-SMC. TNF did not induce apoptosis in Sp-SMC determined by nuclear staining and cellular DNA electrophoresis. In contrast, the reduction of viability in Ep-SMC was associated with induction of apoptosis, as characterized by cellular DNA fragmentation and nuclear condensation. Higher levels of TNF-R1 receptor subtype were detected in membrane preparations from Ep-SMC than in membranes from Sp-SMC. Activation of caspase-3 was also selectively induced in Ep-SMC but not in Sp-SMC. Cycloheximide, an inhibitor of protein synthesis, enhanced the toxicity of TNF in Ep-SMC. This effect of cycloheximide was not seen in Sp-SMC. The data presented here demonstrated for the first time that TNF either promotes growth or induces apoptosis in human VSMC depending on phenotype.
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