SwePub - search: WFRF:(Nabel Elizabeth G)

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1.	Akyürek, Levent, 1966, et al. (author) Deficiency of cyclin-dependent kinase inhibitors p21(Cip1) and p27(Kip1) accelerates atherogenesis in apolipoprotein E-deficient mice. 2010 In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 396:2, s. 359-363 Journal article (peer-reviewed)abstract Cyclin-dependent kinase inhibitors, p21(Cip1)and p27(Kip1), are upregulated during vascular cell proliferation and negatively regulate growth of vascular cells. We hypothesized that absence of either p21(Cip1) or p27(Kip1) in apolipoprotein E (apoE)-deficiency may increase atherosclerotic plaque formation. Compared to apoE(-/-) aortae, both apoE(-/-)/p21(-/-)and apoE(-/-)/p27(-/-) aortae exhibited significantly more atherosclerotic plaque following a high cholesterol regimen. This increase was particularly observed in the abdominal aortic regions. Deficiency of p27(Kip1) accelerated plaque formation significantly more than p21(-/-) in apoE(-/-) mice. This increased plaque formation was in parallel with increased intima/media area ratios. Deficiency of p21(Cip1) and p27(Kip1) accelerates atherogenesis in apoE(-/-) mice. These findings have significant implications for our understanding of the molecular basis of atherosclerosis associated with excessive proliferation of vascular cells.

Akyürek, Levent, 1966, et al. (author)
Deficiency of cyclin-dependent kinase inhibitors p21(Cip1) and p27(Kip1) accelerates atherogenesis in apolipoprotein E-deficient mice.
2010
In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 396:2, s. 359-363
Journal article (peer-reviewed)abstract
- Cyclin-dependent kinase inhibitors, p21(Cip1)and p27(Kip1), are upregulated during vascular cell proliferation and negatively regulate growth of vascular cells. We hypothesized that absence of either p21(Cip1) or p27(Kip1) in apolipoprotein E (apoE)-deficiency may increase atherosclerotic plaque formation. Compared to apoE(-/-) aortae, both apoE(-/-)/p21(-/-)and apoE(-/-)/p27(-/-) aortae exhibited significantly more atherosclerotic plaque following a high cholesterol regimen. This increase was particularly observed in the abdominal aortic regions. Deficiency of p27(Kip1) accelerated plaque formation significantly more than p21(-/-) in apoE(-/-) mice. This increased plaque formation was in parallel with increased intima/media area ratios. Deficiency of p21(Cip1) and p27(Kip1) accelerates atherogenesis in apoE(-/-) mice. These findings have significant implications for our understanding of the molecular basis of atherosclerosis associated with excessive proliferation of vascular cells.

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