(Agencies)
Updated: 2007-12-06 16:30

But there was a problem. Taking heart cells from embryos was feasible in laboratory mice, but unthinkable in humans.

Looking for a substitute that might one day work in people, the researchers performed the same heart operation by grafting skeletal muscular cells taken from the leg of the same animal.

Not only did these new cells fail to protect the heart, they actually made the arrhythmia worse.

The difference, Fleischmann realised, "is that heart muscle electrically couples (with the heart tissue), and skeletal muscle does not."

"This electrical coupling occurs because of a protein called connexin 43," found only in heart cells, he said.

It was this discovery that spawned the idea that holds such promise for heart-attack victims living under the shadow of sudden death. The researchers created a line of mice that "over expressed" connexin 43 in skeletal muscle, and repeated the experiment.

This time, it worked as well as with the embryo heart muscle.

"What is key here is that the cells engrafted into the heart are actually connected to the normal heart cells and activated during the normal beat," said Kotlikoff.

Fleischmann said this could open the way to easy and rapid laboratory production of muscle tissue containing connexin 43.

"You can, so to speak, grow tons of muscle. So one approach would be to do ex-vivo gene therapy," he said, referring to a method of nurturing cells in a lab dish and then transplanting them into the patient.

But the researchers cautioned that there were still many key steps to be taken before the therapy could be tested in humans.

It first needs to be tested in large animals, whose hearts differ significantly from those of mice, they said.

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