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本文引用的文献

1
Absence of p21Waf1/Cip1/Sdi1 modulates macrophage differentiation and inflammatory response and protects against atherosclerosis.p21Waf1/Cip1/Sdi1缺失调节巨噬细胞分化和炎症反应，并预防动脉粥样硬化。
Circulation. 2004 Dec 21;110(25):3830-41. doi: 10.1161/01.CIR.0000148681.01282.89. Epub 2004 Dec 13.
2
Bone marrow-derived immune cells regulate vascular disease through a p27(Kip1)-dependent mechanism.骨髓来源的免疫细胞通过一种依赖p27（Kip1）的机制调节血管疾病。
J Clin Invest. 2004 Aug;114(3):419-26. doi: 10.1172/JCI20176.
3
Cell cycle signaling and cardiovascular disease.细胞周期信号传导与心血管疾病
Cold Spring Harb Symp Quant Biol. 2002;67:163-70. doi: 10.1101/sqb.2002.67.163.
4
Mouse genetic evidence that tranilast reduces smooth muscle cell hyperplasia via a p21(WAF1)-dependent pathway.小鼠遗传学证据表明曲尼司特通过依赖p21（WAF1）的途径减少平滑肌细胞增生。
Arterioscler Thromb Vasc Biol. 2002 Aug 1;22(8):1305-9. doi: 10.1161/01.atv.0000026614.72957.e7.
5
Mutated p21/WAF/CIP transgene overexpression reduces smooth muscle cell proliferation, macrophage deposition, oxidation-sensitive mechanisms, and restenosis in hypercholesterolemic apolipoprotein E knockout mice.突变型p21/WAF/CIP转基因过表达可减少高胆固醇血症载脂蛋白E基因敲除小鼠的平滑肌细胞增殖、巨噬细胞沉积、氧化敏感机制及再狭窄。
FASEB J. 2001 Oct;15(12):2162-70. doi: 10.1096/fj.01-0032com.
6
The growth suppressor p27(Kip1) protects against diet-induced atherosclerosis.生长抑制因子p27（Kip1）可预防饮食诱导的动脉粥样硬化。
FASEB J. 2001 Sep;15(11):1989-95. doi: 10.1096/fj.01-0130com.
7
p27-p16 fusion gene inhibits angioplasty-induced neointimal hyperplasia and coronary artery occlusion.p27-p16融合基因抑制血管成形术诱导的新生内膜增生和冠状动脉闭塞。
Circ Res. 2001 Aug 17;89(4):323-8. doi: 10.1161/hh1601.094482.
8
p27-p16 Chimera: a superior antiproliferative for the prevention of neointimal hyperplasia.p27-p16嵌合体：预防内膜增生的一种更有效的抗增殖剂。
Mol Ther. 2001 Jan;3(1):8-13. doi: 10.1006/mthe.2000.0239.
9
Targeted gene disruption of matrix metalloproteinase-9 (gelatinase B) suppresses development of experimental abdominal aortic aneurysms.基质金属蛋白酶-9（明胶酶B）的靶向基因破坏抑制实验性腹主动脉瘤的发展。
J Clin Invest. 2000 Jun;105(11):1641-9. doi: 10.1172/JCI8931.
10
Proteinases in cardiovascular aneurysms and rupture: targets for therapy?心血管动脉瘤与破裂中的蛋白酶：治疗靶点？
J Clin Invest. 2000 Jun;105(11):1519-20. doi: 10.1172/JCI10242.

细胞周期蛋白依赖性激酶抑制剂 p21Cip1 和 p27Kip1 的缺乏加速载脂蛋白 E 缺陷小鼠的动脉粥样硬化形成。

Deficiency of cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1 accelerates atherogenesis in apolipoprotein E-deficient mice.

机构信息

National Human Genome Research Institute and National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Biochem Biophys Res Commun. 2010 May 28;396(2):359-63. doi: 10.1016/j.bbrc.2010.04.097. Epub 2010 Apr 24.

DOI:10.1016/j.bbrc.2010.04.097
PMID:20417618
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2884298/
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.

摘要

细胞周期蛋白依赖性激酶抑制剂 p21(Cip1)和 p27(Kip1)在血管细胞增殖过程中上调，并负调控血管细胞的生长。我们假设载脂蛋白 E (apoE)-缺陷中 p21(Cip1)或 p27(Kip1)的缺失可能会增加动脉粥样硬化斑块的形成。与 apoE(-/-)主动脉相比，高脂饮食后 apoE(-/-)/p21(-/-)和 apoE(-/-)/p27(-/-)主动脉的动脉粥样硬化斑块明显更多。这种增加尤其出现在腹主动脉区域。与 p21(-/-)相比，p27(Kip1)缺失在 apoE(-/-)小鼠中显著加速了斑块形成。这种增加的斑块形成与内膜/中膜面积比的增加平行。p21(Cip1)和 p27(Kip1)的缺失加速了 apoE(-/-)小鼠的动脉粥样硬化形成。这些发现对我们理解与血管细胞过度增殖相关的动脉粥样硬化的分子基础具有重要意义。