Levels of circulating CD34(+)/VEGFR2(+) and CD133(+)/VEGFR2(+) were significantly higher in the newly diagnosed untreated patients with HL compared to the patients with HL in remission (P = 0.03 and P = 0.005, respectively), in the patients in remission compared to the patients with diabetes (P = 0.011 and P < 0.001, respectively), and in the patients in remission compared to the healthy individuals (P = 0.08 and P = 0.003, respectively).
Moreover, quercetin administration progressively increased the expression of vascular endothelial growth factor (VEGF) and its receptor, VEGFR2 in diabetes rats.
Consequently, the responses of endothelial cells to exogenous VEGF in a mouse model of diabetes were impaired because of a specific deficiency of VEGFR2 at the cell surface, despite a lack of change in transcript abundance.
Angiogenesis impairment in diabetes: role of methylglyoxal-induced receptor for advanced glycation endproducts, autophagy and vascular endothelial growth factor receptor 2.