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

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

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)627-630
Number of pages4
JournalGlycoconjugate Journal
Volume33
Issue number4
DOIs
Publication statusPublished - 2016 Aug 1

Keywords

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

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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