DALLAS, Nov. 8 -- Scientists are finding ways to switch on and off key proteins that may make heart cells come out of biological "dormancy" and replace the damaged cells that result from heart disease. Their research was reported today in two presentations at the American Heart Association's 71st Scientific Sessions.
Unlike most other cells in the body, heart muscle cells, called myocytes, are believed to stop multiplying shortly after birth and do not regenerate, even if they are damaged, say the researchers. Because heart muscle cells can not generate new cells, they enlarge to accommodate growth of the heart and to take over the functioning of cells damaged by a heart attack or other conditions, such as high blood pressure, that stress the heart.
"After a heart attack, or in response to stresses on the heart, myocytes will get bigger. However, these bigger heart cells don't work as well," says W. Robb MacLellan, M.D., assistant professor in the Cardiovascular Research Laboratories at the University of California at Los Angeles School of Medicine.
"We're trying to find a way to get the cells to multiply instead of enlarge," he says. Cells that enlarge cause a condition known as left-ventricular hypertrophy, which can increase the risk of developing congestive heart failure.
MacLellan and colleagues say the research may lead to new "gene therapy" to treat heart enlargement and improve heart function in people who have heart disease.
Based on an earlier study suggesting that the "retinoblastoma" gene was critical
in controlling cell division, MacLellan and his colleagues focused on the
protein that this gene produces retinoblastoma protein, called Rb. Scientists
believe the Rb protein may help keep heart cells "dormant" so they no longer can
divide. To test this theory, MacLellan's group "turned off" the Rb in a group
of mice. Researchers compared heart sizes between the genetically altered mice
and mice who still had the Rb gene o
Contact: Carole Bullock
American Heart Association