Diabetes and obesity are major sources of disability in UK. A common consequence of diabetes is Peripheral Vascular Disease (PVD), represented mainly by limb ischemia and is a principal cause of leg amputation (1). The ischemic insult causes poor blood supply and inflammation. In healthy individuals the inflammation contributes to vascular remodeling, which restores vasculature and blood perfusion, whereas in diabetes this step is impaired leading to poor revascularisation and necrosis (2). The mechanisms behind impaired collateral revascularisation in diabetes are still unclear, but it should require both angiogenesis and arteriolargenesis. Vascular Endothelial Growth Factor (VEGF) is understood to drive angiogenesis, but VEGF mRNA alternative splicing results in both pro- and anti-angiogenic VEGF isoforms (3) Wnt5a has been shown to increase in anti-angiogenic VEGF in circulating monocytes, preventing revascularisation (4). In healthy subjects circulating Wnt5a is inactivated by binding Soluble Frizzled Related Protein (SFRP5); in PVD patients levels of SFRP5 are downregulated (5), allowing Wnt5a to stimulate antiangiogenic VEGF expression. To determine whether sfrp5 contributes to revascularization in ischemia we performed an unilateral hind limb ischemia in SFRP5 knockout mice (SFRP5-/-) or on wild type littermates as control. All animal procedures met the requirements dictated by the Animals (Scientific Procedures) Act 1986 / ASPA Amendment Regulations 2012. Mice were anaesthetized with 2% isofluorane, blood flow was measured using Laser Speckle imaging, the left femoral artery ligated, the animal sutured and recovered. Laser Speckle imaging was carried out on both hindpaws 3 days and then weekly after the ischemia. Mice were killed after 28 and stained for blood vessels with Isolectin B4 and arterioles with smooth muscle actin antibody. Results SFRP5-/- mice had reduced recovery of blood flow after ischemia (figure 1). After 28 days blood flow to the ipsilateral limb mice was 0,84±0,7 of contralateral in SFRP5-/- mice, which was significantly lower than in wild type litter mate controls 0,65±0,06 (Fig 1). Conclusions The finding that Sfrp5-/- mice, which have raised VEGF-A165b expression after hindlimb ischemia, have impaired arteriogenesis (4), indicates that VEGF-A165b may be able to inhibit arteriolargenesis as well as anti-angiogenesis, either directly or indirectly.