One of the important peripheral vascular pathology in diabetes is the decreased collateral vessel formation in the ischemic peripheral limbs. The mechanisms underlying the progression of poor collateral formation after ischemia in diabetes are not completely understood. We recently reported that hyperglycemia-induced protein kinase C delta (PKCd) activation increases the expression of SHP-1, a protein tyrosine phosphatase, which is responsible for PDGF signaling inhibition leading to perivascular cell apoptosis and acellular capillaries in the retina of diabetic rodents. My research team currently use a hind limb ischemia model, to characterize the role of PKC isoforms and SHP-1 activation induced by diabetes and ischemia causing de-phosphorylation and inhibition of PDGF, VEGF and insulin and its subsequent biological abnormalities in capillary formation.