Glyoxalase-1 overexpression partially prevents diabetes-induced impaired arteriogenesis in a rat hindlimb ligation model

作者：Brouwers Olaf; Yu Liang; Niessen Petra; Slenter Jos; Jaspers Karolien; Wagenaar Allard; Post Mark; Miyata Toshio; Backes Walter; Stehouwer Coen; Huijberts Maya; Schalkwijk Casper^*

来源：Glycoconjugate Journal, 2016, 33(4): 627-630.

DOI：10.1007/s10719-016-9681-3

• Glyoxalase-I
• Diabetes
• Arteriogenesis
• Magnetic resonance angiography
• Advanced glycation end-products

We hypothesize that diabetes-induced impaired collateral formation after a hindlimb ligation in rats is in part caused by intracellular glycation and that overexpression of glyoxalase-I (GLO-I), i.e. the major detoxifying enzyme for advanced-glycation-endproduct (AGE) precursors, can prevent this. Wild-type and GLO-I transgenic rats with or without diabetes (induced by 55 mg/kg streptozotocin) were subjected to ligation of the right femoral artery. Laser Doppler perfusion imaging showed a significantly decreased blood perfusion recovery after 6 days in the diabetic animals compared with control animals, without any effect of Glo1 overexpression. In vivo time-of-flight magnetic resonance angiography at 7-Tesla showed a significant decrease in the number and volume of collaterals in the wild-type diabetic animals compared with the control animals. Glo1 overexpression partially prevented this decrease in the diabetic animals. Diabetes-induced impairment of arteriogenic adaptation can be partially rescued by overexpressing of GLO-I, indicating a role of AGEs in diabetes-induced impaired collateral formation.

• 出版日期2016-8