Mesoangioblasts, vessel-associated multipotent stem cells, repair the infarcted heart by multiple cellular mechanisms: a comparison with bone marrow progenitors, fibroblasts, and endothelial cells

Objective—To test the potential of mesoangioblasts (Mabs) in reducing postischemic injury in comparison with bone
marrow progenitor cells (BMPCs), fibroblasts (Fbs), and embryonic stem cell– derived endothelial cells (ECs), and to
identify putative cellular protective mechanisms.
Methods and Results—Cells were injected percutaneously in the left ventricular (LV) chamber of C57BL/6 mice, 3 to 6
hours after coronary ligation, and detected in the hearts 2 days and 6 weeks later. Echocardiographic examinations were
performed at 6 weeks. LV dilation was reduced and LV shortening fraction was improved with Mabs and BMPCs but
not with ECs and Fbs. Donor cell colonization of the host myocardium was modest and predominantly in the smooth
muscle layer of vessels. Capillary density was higher in the peripheral infarct area and apoptotic cardiomyocytes were
fewer with Mabs and BMPCs. Mabs and BMPCs, but not Fbs or ECs, promoted survival of cultured cardiocytes under
low-oxygen in culture. This activity was present in Mab-conditioned medium and could be replaced by a combination
of basic fibroblast growth factor (bFGF), insulin-like growth factor (IGF)-1, and hepatocyte growth factor (HGF), all
of which are produced by these cells. Conditioned medium from Mabs, but not from Fbs, stimulated proliferation of
smooth muscle cells in vitro.
Conclusions—Mabs appear as effective as BMPCs in reducing postinfarction LV dysfunction, likely through production
of antiapoptotic and angiogenic factors. (Arterioscler Thromb Vasc Biol. 2005;25:692-697.)