A protein that the heart produces during its early development reactivates the embryonic coronary developmental program and initiates migration of heart cells and blood vessel growth after a heart attack, researchers at UT Southwestern Medical Center have found.
The molecule, Thymosin beta-4 (TB4), is expressed by embryos during the heart's development and encourages migration of heart cells. The new findings in mice suggest that introducing TB4 systemically after a heart attack encourages new growth and repair of heart cells. The research findings indicate that the molecule affects developmental gene expression as early as 24 hours after systemic injection. The UT Southwestern study is online and will appear in an upcoming issue of the Journal of Molecular and Cellular Cardiology.
"This molecule has the potential to reprogram cells in the body to get them to do what you want them to do," said Dr. J. Michael DiMaio, associate professor of cardiothoracic surgery at UT Southwestern and senior author of the study. Obviously, the clinical implications of this are enormous because of the potential to reverse damage inflicted on heart cells after a heart attack."
Tremendous medical progress has been made to counter the damaging effects of heart attacks, but ordinarily, mammalian hearts are incapable of repairing themselves following damage. They are also limited in their ability to form new blood vessels. Earlier studies demonstrated that TB4 is expressed in the embryonic heart and stimulates cardiac vessels to form. It was therefore thought that introduction of TB4 might activate new vessel growth in the adult heart.
In this mouse study researchers found that TB4 initiates capillary tube formation of adult coronary endothelial cells in tissue culture. The molecule also encourages cardiac regeneration by inhibiting death in heart cells after an injury such as a heart attack and by stimulating new vessel growth.