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Healing hearts

发布时间:2019-03-08 04:13:02来源:未知点击:

By Nell Boyce UNLIKE most cells in the body, heart cells lose their ability to divide and multiply soon after birth. But by tinkering with genes, researchers have created mice whose hearts don’t lose this ability. They say the discovery could pave the way for treating heart failure using gene therapy. Cells with extremely specialised structures, such as neurons and heart cells, find it difficult to divide. So when heart cells die because of a blood clot or high blood pressure, other cells compensate by growing larger. However, these swollen cells cannot pump as effectively as healthy cells, and the heart will eventually fail even if patients take drugs to lower their blood pressure. Finding a way to make cells divide after a heart injury would solve the problem. At last week’s meeting, Robb MacLellan of the University of California at Los Angeles described his work with genetically engineered mice whose hearts lacked a key gene called retinoblastoma. This gene is known to suppress cell division in many tissues. At the age of eight weeks, the genetically engineered mice had hearts 8 per cent larger than mice with normal hearts, because of continuing cell division. And the heart cells did not stop dividing until the mice were 20 weeks old. MacLellan and his colleagues say they have also identified a protein called MRP1 that appears to block the effects of retinoblastoma in heart tissue. They believe that this protein may be able to start cell division in the mouse hearts again. “There’re glimmers of hope in preliminary results in a number of labs,” says Loren Field from the Indiana University School of Medicine in Indianapolis. He and his colleagues have shown that overexpression of two genes known as cyclin D-1 and TSC2 can prompt heart cells to enter the initial stages of the cell division cycle. But the most important step will be for scientists to show that heart cells can proliferate after an injury, and to follow the progress of the resulting cells to check that they remain healthy, according to Field. “A lot of these genetic manipulations are markedly increasing the numbers of cells producing DNA in the heart,” he says. “But what’s the fate of these cells?” Michael Schneider of Baylor College of Medicine in Houston, who also studies proteins involved in cell division, agrees that it is relatively easy to get heart cells to take the first step towards division and duplicate the chromosomes, but that the later steps are proving more elusive. “The idea that everything would flow like water over a waterfall isn’t the case here,” says Schneider. However,