Figure 3: Schematic illustrations of effects of hMSCs on ligated carotid artery (a) and inflammatory cytokines on injured artery (b). Systemic administration of hMSCs decreased neointimal hyperplasia in mouse model without significant long-term engraftment into lesion (a). Rather, modulation of inflammatory response conferred therapeutic benefits. Inflammatory cytokines signal a need for repair and mobilized endogenous bone marrow cells play an important role in neointimal hyperplasia development after vascular injury (b). Inflammatory cytokines might contribute to activation, migration, and proliferation of smooth muscle progenitor cells at sites of injury, through mobilization of bone-marrow-derived cells.