Following a myocardial infarction (MI), cells such as mast cells, bone marrow stem cells, and fibroblasts play a role in tissue regeneration and wound healing. Cardiac-resident fibroblasts phenotypically convert to myofibroblasts, which have characteristics of smooth muscle cells and exert contractile force to help prevent infarct expansion and ventricular dilatation. Myofibroblasts can also be driven from other sources, including bone marrow-derived mesenchymal stem cells (MSCs). Previous work in our lab showed that mast cell deficient (c-kit deficient) mice undergo rapid ventricular dilatation compared with wild-type mice and accumulate fewer myofibroblasts in the infarct region post-MI. Therefore, mast cells may play an important role in myofibroblast accumulation in response to cardiac injury. We investigated the role of mast cells and miR-145 and miR-143 in the proliferation and differentiation of MSCs to myofibroblasts since miR-145 and miR-143 have been shown to be involved in the regulation of smooth muscle phenotype.