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Hyperglycaemia is associated with impaired vasa vasorum neovascularization and accelerated atherosclerosis in apolipoprotein-E deficient mice.

Abstract：

OBJECTIVE:A direct correlation between blood glucose levels and the microvascular complications of diabetes is well established. However, the effects of hyperglycaemia on the vasa vasorum, a microvascular network which surrounds and supplies the walls of large arteries, is not known. The objective of this study is to investigate the effects of hyperglycaemia on the vasa vasorum and to examine correlations between these effects and the development of atherosclerosis in a mouse model. METHODS:The micro- and macrovascular effects of hyperglycaemia were examined in streptozotocin-injected apolipoprotein-E deficient (ApoE(-/-)) mice. Retina and aortic sinus were isolated from hyperglycaemic mice and normoglycaemic controls at 5-20 weeks of age. Retinal and vasa vasorum microvessel densities were quantified and correlated to atherosclerotic lesion development. The expression levels of pro-angiogenic factors including vascular endothelial growth factor (VEGF) and VEGF receptor 2 were examined. RESULTS:In normoglycaemic ApoE(-/-) mice atherogenesis is associated with vasa vasorum expansion, which likely corresponds to the increasing blood supply demands of the thickening artery wall. In hyperglycaemic ApoE(-/-) mice there is no significant neovascularization of the vasa vasorum, despite the fact that lesions are significantly larger. This defect may result from a localized deficiency in VEGF. CONCLUSIONS:These findings are the first evidence that hyperglycaemia alters the structure of the vasa vasorum. Such microvascular changes directly correlate, and may contribute to, the development and progression of atherosclerosis in hyperglycaemic ApoE-deficient mice.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Veerman KJ,Venegas-Pino DE,Shi Y,Khan MI,Gerstein HC,Werstuck GH

doi

10.1016/j.atherosclerosis.2013.01.018

subject

Has Abstract

pub_date

2013-04-01 00:00:00

pages

250-8

issue

2

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(13)00053-1

journal_volume

227

pub_type

杂志文章

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