Implanting embryonic cardiac cells prevents a...( When researchers at Cornell the Univ...)

When researchers at Cornell, the University of Bonn and the University of Pittsburgh transplanted living embryonic heart cells into cardiac tissue of mice that had suffered heart attacks, the mice became resistant to cardiac arrhythmias, thereby avoiding one of the most dangerous and fatal consequences of heart attacks.

The discovery, reported in this week's issue of Nature, has profound implications for using cell-transplant therapies to restore damaged heart tissue.

The researchers, including Michael Kotlikoff, the Austin O. Hooey Dean of Cornell's College of Veterinary Medicine, one of the paper's senior authors, 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.

Scientists recognize the untapped potential of using cell-based therapies to counter many debilitating diseases, but they have not had tools to assess the function of the cells once transferred. In Kotlikoff's laboratory, the researchers determined that the transplanted embryonic cells were making electrical connections with normal heart cells. Using genetically modified heart cells that express a fluorescent sensor, they established that transplanted heart cells were activated during norm
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