Hyperglycemia Degrades the Endothelial Glycocalyx Through a Decrease in Syndecan-1

• Emma Hudgins, Biochemistry, University of Delaware

• Ibra Fancher, Kinesiology and Applied Physiology, University of Delaware

Although endothelial dysfunction is known to be associated with obesity, the mechanisms causing the dysfunction are not well understood. The glycocalyx is an extracellular matrix present in endothelial cells that has been shown to play a role in endothelial cell function. It is composed of glycosaminoglycans anchored to membrane proteins such as Glypican-1, which is thought to play a role in mechanosensing, and Syndecan-1, which has been shown to be involved in physiological endothelial function. To assess the effect of hyperglycemia on the glycocalyx, cultured endothelial cells were treated with high levels of glucose. Gene expression was assessed with PCR, and protein expression was evaluated with Western blot and fluorescent immunostaining.  No change was observed in either Glypican-1 or Syndecan-1 gene expression after exposure to high glucose. Western blot showed a decrease in whole-cell Syndecan-1 expression after glucose treatment, and immunocytochemistry data showed a similar decrease in membrane expression of Syndecan-1. No significant change was noted in whole-cell or membrane protein expression of Glypican-1. This may suggest that hyperglycemia contributes to endothelial dysfunction by degrading the glycocalyx through a decrease in Syndecan-1. Further experiment is needed to determine whether this decrease is due to a downregulation of translation or an increase in Syndecan-1 shedding.