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周细胞与糖尿病视网膜病变的发病机制

Pericytes and the pathogenesis of diabetic retinopathy.

作者信息

Hammes Hans-Peter, Lin Jihong, Renner Oliver, Shani Moshe, Lundqvist Andrea, Betsholtz Christer, Brownlee Michael, Deutsch Urban

机构信息

Fifth Medical Clinic, Medical Faculty of the University of Heidelberg, Mannheim, Germany.

出版信息

Diabetes. 2002 Oct;51(10):3107-12. doi: 10.2337/diabetes.51.10.3107.

Abstract

Pericytes provide vascular stability and control endothelial proliferation. Pericyte loss, microaneurysms, and acellular capillaries are characteristic for the diabetic retina. Platelet-derived growth factor (PDGF)-B is involved in pericyte recruitment, and brain capillaries of mice with a genetic ablation of PDGF-B show pericyte loss and microaneurysms. We investigated the role of capillary coverage with pericytes in early diabetic retinopathy and the contribution to proliferative retinopathy using mice with a single functional allele of PDGF-B (PDGF-B(+/-) mice). As assessed by quantitative morphometry of retinal digest preparations, pericyte numbers in nondiabetic PDGF-B(+/-) mice were reduced by 30% compared with wild-type mice, together with a small but significant increase in acellular capillaries. Pericyte numbers were reduced by 40% in diabetic wild-type mice compared with nondiabetic wild-type controls. Pericyte numbers were decreased by 50% in diabetic PDGF-B(+/-) mice compared with nondiabetic wild-type littermates, and the incidence of acellular capillaries was increased 3.5-fold when compared with nondiabetic PDGF-B(+/-) mice. To investigate the effect of pericyte loss in the context of ongoing angiogenesis, we subjected mice to hypoxia-induced proliferative retinopathy. As a result, PDGF-B(+/-) mice developed twice as many new blood vessels as their wild-type littermates. We conclude that retinal capillary coverage with pericytes is crucial for the survival of endothelial cells, particularly under stress conditions such as diabetes. At high vascular endothelial growth factor levels, such as those in the retinopathy of prematurity model, pericyte deficiency leads to reduced inhibition of endothelial proliferation in vivo.

摘要

周细胞为血管提供稳定性并控制内皮细胞增殖。周细胞丢失、微动脉瘤和无细胞毛细血管是糖尿病视网膜病变的特征。血小板衍生生长因子(PDGF)-B参与周细胞募集,PDGF-B基因敲除小鼠的脑毛细血管出现周细胞丢失和微动脉瘤。我们使用具有单个功能性PDGF-B等位基因的小鼠(PDGF-B(+/-)小鼠),研究了周细胞对毛细血管的覆盖在早期糖尿病视网膜病变中的作用以及对增殖性视网膜病变的影响。通过对视网膜消化制剂的定量形态学评估,与野生型小鼠相比,非糖尿病PDGF-B(+/-)小鼠的周细胞数量减少了30%,同时无细胞毛细血管有少量但显著增加。与非糖尿病野生型对照相比,糖尿病野生型小鼠的周细胞数量减少了40%。与非糖尿病野生型同窝小鼠相比,糖尿病PDGF-B(+/-)小鼠的周细胞数量减少了50%,与非糖尿病PDGF-B(+/-)小鼠相比,无细胞毛细血管的发生率增加了3.5倍。为了研究在持续血管生成情况下周细胞丢失的影响,我们使小鼠发生缺氧诱导的增殖性视网膜病变。结果,PDGF-B(+/-)小鼠形成的新血管数量是其野生型同窝小鼠的两倍。我们得出结论,周细胞对视网膜毛细血管的覆盖对于内皮细胞的存活至关重要,尤其是在糖尿病等应激条件下。在高血管内皮生长因子水平下,如早产儿视网膜病变模型中的水平,周细胞缺乏导致体内对内皮细胞增殖的抑制作用减弱。

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