Endothelial Progenitor Cells in Diabetic Microvascular Complications: Friends or Foes?

Figure 1

Uncoupling VEGF with nitric oxide in microvascular endothelial cells. Hyperglycemia promoted local VEGF production. VEGF stimulated endothelial cell proliferation via binding to VEGFR2. It induced endothelial cell migration and altered junction complex, in particular, VE-cadherin on the membrane. In parallel, VEGF promoted ICAM1 expression in endothelial cells which triggered inflammatory response to attack endothelium and made VE-cadherin dissemble. ICAM1 could also enhance ROS production that has negative impact on nitric oxide level and bioavailability. Although VEGF promoted nitric oxide production in endothelial cells via its receptor Flt1, nitric oxide is significantly reduced by ROS and oxidative stress, losing its inhibitory effect on VEGF-induced endothelial cell proliferation, migration, and activation.