Analysis of the Therapeutic Potential of Stem Cells to Facilitate Recovery from Cardiac Disease and Damage.

摘要

Heart disease is the leading cause of death in both the United States and Hawaii, including men and women of the Armed Forces. Furthermore, chest trauma in military men and women can lead to cardiac injury and cardiomyopathy. There is presently no good therapy for injured myocardium. Stem cells hold great promise in the field of regenerative medicine, and may be the key to developing new therapies to treat cardiac damage. Our prior study showed that blood stem cells can, to some extent, facilitate repair of cardiac damage in a mouse model of cardiac infarct. Adipose stem cells however, are more accessible and abundant than blood stem cells, and are multipotent(can produce several different tissues types other than adipose). The latter property may make directed re-programming of these cells into the cardiac lineage more efficient. The objectives for the present study are: (No. 1) Test the hypothesis that the multipotent adipose-derived stem cells will perform better than bone marrow- derived stem cells in facilitating recovery from heart disease. (No. 2) Test the hypotheses that cardiac-like progenitors, derived via reprogramming of different types of stem cells, will further enhance the therapeutic potential of stem cell-based methodologies in the treatment of heart disease and (No. 3), the delivery of re-programming factors into stem cells using a transposase-mediated gene delivery system will enhance the re-programming efficiency of stem cells towards the cardiac lineage. The results to date have confirmed that adipose stem cells may be re-programmed into the cardiac lineage with an efficiency of (approximately) 25%, substantially higher than (approximately) 1% efficiency we had previously observed for blood stem cells. We are presently working an analysis of the relative potential of adipose stem cells and reprogrammed adipose stem cells to facilitate recovery of induced infarcts in our murine model.