The possible mechanism for impaired angiogenesis after transient focal ischemia in type 2 diabetic GK rats: different expressions of angiostatin and vascular endothelial growth factor.

BACKGROUND

The development of collateral vessels, which is important to prevent ischemic tissues from cell death, is impaired in patients with diabetes mellitus. The process is regulated by many positive and negative factors. The purpose of the study is to test the hypothesis that stroke patients with diabetes have angiogenesis deficiency and the possible mechanism is hyperglycemia attenuates neovascularization by downregulating proliferative properties of vascular endothelial growth factor (VEGF) and upregulating negative properties of angiostatin.

METHODS

Diabetes groups [Goto-Kakizaki (GK)] and respective controls (Wistar rats) underwent 1.5h of middle cerebral artery occlusion (MCAO) and then reperfused for 24h and 7d. Immunohistochemistry was used to describe the change of vessel density. The expression levels of VEGF and angiostatin were estimated by western blot.

RESULTS

Compared with the controls, the diabetes groups had lower vessel density, more expression of angiostatin, and lower level of VEGF.

CONCLUSIONS

These results showed angiogenesis was deficient in diabetes groups after ischemic reperfusion (I/R) injury. And the possible mechanism is hyperglycemia attenuates neovascularization by downregulating proliferative properties of VEGF and upregulating of negative properties of angiostatin.