Loss of CDKN2B promotes p53-dependent smooth muscle cell apoptosis and aneurysm formation.

ABSTRACT:

Objective

Genomewide association studies have implicated allelic variation at 9p21.3 in multiple forms of vascular disease, including atherosclerotic coronary heart disease and abdominal aortic aneurysm. As for other genes at 9p21.3, human expression quantitative trait locus studies have associated expression of the tumor suppressor gene CDKN2B with the risk haplotype, but its potential role in vascular pathobiology remains unclear.

Methods and results

Here we used vascular injury models and found that Cdkn2b knockout mice displayed the expected increase in proliferation after injury, but developed reduced neointimal lesions and larger aortic aneurysms. In situ and in vitro studies suggested that these effects were attributable to increased smooth muscle cell apoptosis. Adop

SUBMITTER: Leeper NJ 

PROVIDER: S-EPMC3569043 | biostudies-literature | 2013 Jan

REPOSITORIES: biostudies-literature