The research team from Cornell University, the University of Pittsburgh and the University of Bonn, Germany, discovered that a protein called connexin43, expressed by the transplanted embryonic heart cells, improved electrical connections to other heart cells. The researchers showed that the improved connections helped activate the transplanted cells deep within the damaged section of the heart tissue. The technique reversed the risk of developing ventricular arrhythmias after a heart attack, the number one cause of sudden death in the Western world.
In the past, scientists have transplanted a variety of cell types into failing hearts with modest improvement of function, although transplanting skeletal muscle cells made things worse and led to more arrhythmias. Surprisingly, when co-author Bernd Fleischmann at the University of Bonn and colleagues transplanted embryonic cardiac cells, the hearts' electrical stability and function returned to normal.
The researchers used genetically modified heart cells that express a fluorescent sensor, they established that transplanted heart cells were activated during normal heart contractions. Professor Guy Salama at the University of Pittsburgh School of Medicine was also able to map voltage signals across the surface of the hearts, establishing that the implanted cells improve conduction of electrical signals within the damaged heart tissue. While doctors could never use cells from a human embryonic heart for transplantation, researchers at the University of Bonn engineered skeletal muscle to express connexin43 and achieved the same restorative results as they did with the embryonic heart cells.
MEDICA.de; Source: Cornell University