| First Author | Guevara NV | Year | 1999 |
| Journal | Nat Med | Volume | 5 |
| Issue | 3 | Pages | 335-9 |
| PubMed ID | 10086392 | Mgi Jnum | J:53309 |
| Mgi Id | MGI:1332283 | Doi | 10.1038/6585 |
| Citation | Guevara NV, et al. (1999) The absence of p53 accelerates atherosclerosis by increasing cell proliferation in vivo. Nat Med 5(3):335-9 |
| abstractText | The tumor suppressor protein p53 is an essential molecule in cell proliferation and programmed cell death (apoptosis), and has been postulated to play a principal part in the development of atherosclerosis. We have examined the effect of p53 inactivation on atherogenesis in apoE-knockout mice, an animal model for atherosclerosis. We found that, compared with p53+/+/apoE-/- mice, p53-/-/apoE-/- mice developed considerably accelerated aortic atherosclerosis in the presence of a similar serum cholesterol in response to a high-fat diet. Furthermore, the atherosclerotic lesions in p53-/-/apoE-/- mice had a significant (approximately 280%) increase in cell proliferation rate and an insignificant (approximately 180%) increase in apoptosis compared with those in p53+/+/apoE-/- mice. Our observations indicate that the role of p53 in atherosclerotic lesion development might be associated with its function in cell replication control, and that p53-independent mechanisms can mediate the apoptotic response in atherosclerosis. |
