Title : Ameliorating Methylglyoxal-Induced Progenitor Cell Dysfunction for Tissue Repair in Diabetes.

Pub. Date : 2019 Jun

PMID : 30885990






4 Functional Relationships(s)
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1 We hypothesized that the MGO scavenger glyoxalase 1 (GLO1) reverses bone marrow-derived PC (BMPC) dysfunction through augmenting the activity of an important endoplasmic reticulum stress sensor, inositol-requiring enzyme 1alpha (IRE1alpha), resulting in improved diabetic wound healing. Pyruvaldehyde glyoxalase 1 Mus musculus
2 We hypothesized that the MGO scavenger glyoxalase 1 (GLO1) reverses bone marrow-derived PC (BMPC) dysfunction through augmenting the activity of an important endoplasmic reticulum stress sensor, inositol-requiring enzyme 1alpha (IRE1alpha), resulting in improved diabetic wound healing. Pyruvaldehyde glyoxalase 1 Mus musculus
3 MGO at the concentration of 10 micromol/L induced immediate and severe BMPC dysfunction, including impaired network formation, migration, and proliferation and increased apoptosis, which were rescued by adenovirus-mediated GLO1 overexpression. Pyruvaldehyde glyoxalase 1 Mus musculus
4 In conclusion, our data suggest that GLO1 rescues BMPC dysfunction and facilitates wound healing in diabetic animals, at least partly through preventing MGO-induced impairment of IRE1alpha expression and activity. Pyruvaldehyde glyoxalase 1 Mus musculus