Vascular smooth muscle cell growth kinetics in vivo in aged rats

M. B. Stemerman, R. Weinstein, J. W. Rowe, T. Maciag, R. Fuhro, R. Gardner

Research output: Contribution to journalArticlepeer-review

100 Scopus citations

Abstract

Age is risk factor in the development of atherosclerosis. In this study we investigated the hypothesis that proliferation of vascular smooth muscle cells (SMCs), an integral part of atherosclerosis plaque formation, changes with age. SMC growth kinetics of old rats (21-24 months) were compared to those of young adult rats (3-4 months). Rat aortas were denuded of their endothelium and the animals were killed after [3H] thymidine and Evans blue injections at 0-28 days after denudation. Incorporation of [3H] thymidine into SMC peaked in the young animals by day 2, whereas the older animals responded to endothelial removal with greater incorporation at day 2 and a more sustained rate of incorporation peaking at day 4. The [3H] thymidine incorporation curves decreased sharply from their peaks at 2 and 4 days, respectively, and paralleled each other after day 7. [3H] Thymidine uptake reflected the subsequent SMC intimal growth as measured morphometrically, with old animals showing greater numbers of intimal SMC than did the younger animals. The difference in response of SMC to injury with age suggests that aging producers a change in the vascular SMC that enhances proliferation. This change in response implies that the more pronounced atherosclerotic plaque growth seen with aging may be a result of an age-related increase in response to injury rather than merely the accumulation of time-related intimal change.

Original languageEnglish
Pages (from-to)3863-3866
Number of pages4
JournalProceedings of the National Academy of Sciences of the United States of America
Volume79
Issue number12 I
DOIs
StatePublished - 1982
Externally publishedYes

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