Glycophosphatidylinositol (GPI)-anchored proteins are one of the membrane-bound proteins that have diverse functions. There have been some reports that their expression or activities are altered in diabetes. Many proteins, including GPI-anchored proteins, lose their biological function secondary to carbonylation in diabetes. Carbonylation causes oxidative damage of numerous proteins in the human body. Diabetic complications are related to carbonyl adducts in vascular tissue. Therefore, we examined whether carbonyl compounds associated with diabetes affect the expression of GPI-related genes in human umbilical vein endothelial cells (HUVECs). Among the more than 150 GPI anchor-related genes investigated, 54 genes were up-regulated by more than 2-fold, while 31 genes were down-regulated with altered expression levels of 2-fold in acrolein (ACR)-treated cells. The majority of the genes changed by ACR involved GPI anchor biosynthesis. Crotonaldehyde and methylglyoxal altered a few genes encoding GPI-anchored proteins. According to their functional characteristics, genes were classified into the Gene Ontology functional categories. We also identified the distribution of functional groups of GPI anchor-related genes in HUVECs. In conclusion, our data suggest that these reactive carbonyl compounds modulate GPI anchor-related gene expression, which may have a role in diabetic vasculopathy.
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Yang, H., Lee, S.E., Jeong, S.I. et al. Differentially-expressed genes associated with glycophosphatidylinositol (GPI)-anchored proteins by diabetes-related toxic substances in human endothelial cells. BioChip J 6, 262–270 (2012). https://doi.org/10.1007/s13206-012-6309-y
- GPI-anchored protein
- Endothelial cell