Decreased Circulating Progenitor Cell Number and Failed Mechanisms of Stromal Cell-Derived Factor-1 Mediated Bone Marrow Mobilization Impair Diabetic Tissue Repair

neovascularization and tissue repair. Here, we explore the mech-anism contributing to decreased diabetic circulating PC number and propose a novel treatment to restore circulating PC number, peripheral neovascularization, and tissue healing. RESEARCH DESIGN AND METHODS—Cutaneous wounds were created on wild-type (C57BL/J6) and diabetic (Leprdb/db) mice. Blood and bone marrow PCs were collected at multiple time points. RESULTS—Significantly delayed wound closure in diabetic animals was associated with diminished circulating PC number (1.9-fold increase vs. 7.6-fold increase in lin/sca-1/ckit in wild-type mice; P 0.01), despite adequate numbers of PCs in the bone marrow at baseline (14.4 3.2 % lin/ckit/sca1 vs. 13.5 2.8 % in wild-type). Normal bone marrow PC mobilization in response to peripheral wounding occurred after a necessar