Abstract 941: The Human Umbilical Cord Blood- and Adipose Tissue-Derived Mesenchymal Stem Cells Improve Function of Infarcted Myocardium
Background: Cell therapy using mesenchymal stem cell (MSC) to ischemic heart diseases is in fast progress. Besides of bone marrow, umbilical cord blood (UCB) and adipose tissue (AT) are recently interested as a source of MSC due to their easy accessibility. We elucidated the potentials of human UCB and AT derived MSCs for myocardial tissue repair in a model of extensive myocardial infarction.
Methods: MSCs were successfully isolated and characterized from human UCB and AT. Myocardial infarction was induced by ligation of left anterior descending coronary artery for 30 minutes followed by release in rats. Cells (1–2 x 106) or media only (control) were injected in a 3 designated points around the infarcted area and immunosuppressive agent using cyclosporin were treated during follow-up time. Before and 4 weeks after injection, the echocardiography was performed. Tracking of human cells was performed by in situ hybridization for human X and Y chromosomes and bioluminescence imaging. And histological studies were performed by H&E, masson trichrome staining, and immunohistochemisty.
Results: In situ hybridization and bioluminescence imaging revealed transplanted human-derived MSCs were engrafted in the myocardium. Myocardial fibrosis was significantly decreased in UCB and AD derived MSC-treated infarcted myocardium compared with control one. Scar tissue from cell-treated animals was significantly populated with cardiomyocyte like cells indicated by alpha-smooth muscle actin staining. In echocardiographic findings 4 weeks after injections, fractional shortening (FS) was 33.1±11.0 % and 37±8.4 % (n=5, in each), and ejection fraction (EF) was 69.3±13.1 % and 65.7±14.2 % (n=5, in each) in UCB and AD derived MSCs injected rats (p<0.05, p<0.05 vs. control FS; 17.2±8.5 %, and control EF; 40.6±17.5%, n=5).
Conclusion: Both UCB and AD derived MSCs are another candidate for improvement of the left ventricular (LV) function in a rat myocardial infarction model. The detailed mechanism for improved LV function will be presented.