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Glycoconj J. 2016 Aug;33(4):627-30. doi: 10.1007/s10719-016-9681-3. Epub 2016 Jun 13.

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

Author information

1
Department of Internal Medicine, Laboratory for Metabolism and Vascular Medicine, Maastricht University Medical Center, P.O. Box 5800, 6202, AZ, Maastricht, The Netherlands.
2
Department of Radiology, Maastricht University Medical Centre, Universiteitssingel 50, Maastricht, the Netherlands.
3
Department of Physiology, Maastricht University Medical Centre, Universiteitssingel 50, Maastricht, the Netherlands.
4
Centre of Translational and Advanced Research, Tohoku University, Sendai, Miyagi Prefecture, 980-8577, Japan.
5
Department of Internal Medicine, Laboratory for Metabolism and Vascular Medicine, Maastricht University Medical Center, P.O. Box 5800, 6202, AZ, Maastricht, The Netherlands. c.schalkwijk@maastrichtuniversity.nl.

Abstract

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.

KEYWORDS:

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

PMID:
27296676
PMCID:
PMC4975762
DOI:
10.1007/s10719-016-9681-3
[Indexed for MEDLINE]
Free PMC Article

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