Mechanism of Hoxa3 induction of proangiogenic Gr-1⁺CD11b⁺ myeloid cells and their contribution to injury-induced neovascularization and wound healing. Injury results in mobilization and recruitment of BMD stem/progenitor cells to the site of injury. Overexpression of Hoxa3 at the site of injury promotes the differentiation of BMD stem/progenitor cells into granulocytic Gr-1⁺CD11b⁺ cells, which promote neovascularization through the various mechanisms shown. Hoxa3 also rescues at least some of the aberrant phenotypes, such as defective migratory and adhesive properties, of Gr-1⁺CD11b⁺ cells in pathological conditions such as diabetes.