Dan Yang and Donald J. McCrann contributed equally to this paper.
Increased polyploidy in aortic vascular smooth muscle cells during aging is marked by cellular senescence
Article first published online: 15 JAN 2007
Volume 6, Issue 2, pages 257–260, April 2007
How to Cite
Yang, D., McCrann, D. J., Nguyen, H., Hilaire, C. St., DePinho, R. A., Jones, M. R. and Ravid, K. (2007), Increased polyploidy in aortic vascular smooth muscle cells during aging is marked by cellular senescence. Aging Cell, 6: 257–260. doi: 10.1111/j.1474-9726.2007.00274.x
- Issue published online: 5 FEB 2007
- Article first published online: 15 JAN 2007
- Accepted for publication 6 December 2006
- cellular senescence;
- senescence-associated β-galactosidase;
- vascular smooth muscle
We previously reported that the frequency of polyploid aortic vascular smooth muscle cells (VSMC) serves as a biomarker of aging. Cellular senescence of somatic cells is another marker of aging that is characterized by the inability to undergo cell division. Here, we examined whether polyploidy is associated with the development of cellular senescence in vivo. Analysis of aortic tissue preparations from young and old Brown Norway rats showed that expression of senescence markers such as p16INK4a and senescence-associated β-galactosidase activity are detected primarily in the old tissues. VSMC from p16INK4a knockout and control mice display similar levels of polyploid cells. Intriguingly, senescence markers are expressed in most, but not all, polyploid VSMC. Moreover, the polyploid cells exhibit limited proliferative capacity in comparison to their diploid counterparts. This study is the first to demonstrate in vivo that polyploid VSMC adopt a senescent phenotype.