Glycation by glyoxal leads to profound changes in the behavior of dermal fibroblasts

Introduction Diabetes is a worldwide health problem that associated with severe complications. Advanced Glycation End products (AGEs) such as Nε-(carboxymethyl)lysine, which result from chronic hyperglycemia, accumulate in the skin of patients diabetes. The effect AGEs on fibroblast functionality and their impact wound healing are still poorly understood. Research design methods To investigate this, we treated cultured human fibroblasts 0.6 mM glyoxal to induce acute glycation. behavior was analyzed by time-lapse monolayer wounding assay, seahorse technology atomic force microscopy. Production extracellular matrix studied transmission electronic microscopy western blot. Lipid metabolism investigated staining lipid droplets (LDs) BODIPY 493/503. Results We found proliferative migratory capacities cells were greatly reduced glycation, could be explained an increase tensile strength. Measurement cellular energy balance did not indicate there change rate oxygen consumption fibroblasts. Assessment collagen I revealed influence type secretion although it disrupt maturation prevented its deposition matrix. noted pronounced number LDs after treatment. AMPK phosphorylation treatment but responsible for accumulation LDs. Conclusion Glyoxal promotes favor lipogenic activity involved delaying healing.