Apoptosis of human vascular smooth muscle cells derived from normal vessels and coronary atherosclerotic plaques - PubMed (original) (raw)
Comparative Study
. 1995 May;95(5):2266-74.
doi: 10.1172/JCI117917.
Affiliations
- PMID: 7738191
- PMCID: PMC295839
- DOI: 10.1172/JCI117917
Comparative Study
Apoptosis of human vascular smooth muscle cells derived from normal vessels and coronary atherosclerotic plaques
M R Bennett et al. J Clin Invest. 1995 May.
Abstract
We studied death of human vascular smooth muscle cells derived from coronary plaques and normal coronary arteries and aorta. Cells from normal arteries underwent death only upon removal of serum growth factors. In contrast, plaque-derived cells died even in high serum conditions, and death increased after serum withdrawal. Death was characteristically by apoptosis in both normal and plaque-derived cells, as determined by time-lapse videomicroscopy, electron microscopy, and DNA fragmentation patterns. IGF-1 and PDGF were identified as potent survival factors in serum, whereas EGF and basic fibroblast growth factor had little effect. Stable expression of bcl-2, a protooncogene that regulates apoptosis in other cell lines, protected smooth muscle cells from apoptosis, although there was no detectable difference in endogenous bcl-2 expression between cells from plaques or normal vessels. We conclude that apoptosis of human vascular smooth muscle cells is regulated by both specific gene products and local cytokines acting as survival factors. Apoptosis may therefore regulate cell mass in the normal arterial wall and the higher rates of apoptosis seen in plaque smooth muscle cells may ultimately contribute to plaque rupture and breakdown and thus to the clinical sequelae of atherosclerosis.
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