Deficiency of cyclin-dependent kinase inhibitors p21(Cip1) and p27(Kip1) accelerates atherogenesis in apolipoprotein E-deficient mice.

Akyürek, Levent, 1966 (author): Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology

Boehm, Manfred (author)

Olive, Michelle (author)

Zhou, Xianghua, 1973 (author): Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology

San, Hong (author)

Nabel, Elizabeth G (author)

(creator_code:org_t)

Elsevier BV, 2010
2010
English.
In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 396:2, s. 359-363

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Abstract Subject headings

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.

By the author/editor: Akyürek, Levent, ...; Boehm, Manfred; Olive, Michelle; Zhou, Xianghua, ...; San, Hong; Nabel, Elizabeth ...

About the subject

MEDICAL AND HEALTH SCIENCES: MEDICAL AND HEAL ...; and Basic Medicine; and Cell and Molecul ...

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