The accumulation of old cells, the stagnation in the body is to blame for diseases related to age, a new study has found. When researchers removed these mouse cells, they were able to delay the onset of cataracts and slow muscle loss related to age.
"This really is a technical tour de force," says geneticist Norman Sharpless of the University of North Carolina School of Medicine in Chapel Hill, who was not involved in the study. "And then they went beyond this technical feat and made findings that are really important to understand the basic science of aging."
Most cells of the body can not continue to divide forever. After a cell itself duplicated a number of times around 50 is the average genetic switch disables division program. A cell that is better known under the division name is senescent; he continues to live, but no longer works as it once did. While most senescent cells continue to behave as any cell type, they started as they also begin to secrete immune proteins that scientists have speculated could cause changes related to age in the surrounding tissues . In elderly humans, at least 5% of total cells in the body are thought to be senescent. The cells accumulate in areas particularly affected by aging-eyes and muscles, for example.
"It has been hypothesized, since these cells are on pathologies of the sites associated with age, they are linked to the development of these diseases," says biologist Jan van Deursen of the Mayo Clinic in Rochester, Minnesota, lead author of the new paper. But the connection has not been fully expanded, he said.
Van Deursen and colleagues have developed a way to kill the senescent cells in mice, delete them from the body. They designed mice so that when the cells returned to a known gene p16 Ink4a , a marker of senescence, the cell would also turn on the production of inactive cell death genes, not normally produced by senescent cells. Then, when the researchers gave the mice a drug, the way of death would be activated in all senescent cells. "Our method allowed us to look at the consequences of the removal of senescent cells at different stages of mouse life cycle, "said van Deursen. "We are not simply block senescence altogether."
First, the researchers cleared senescent cells of all mice throughout their lives, giving the drug every 3 days beginning when the animals were weaned. Although the mouse does not have a longer life, the appearance of the cataract has been delayed for about 100 days, the treated mice had muscle fiber twice as wide, and their curvature and fat deposits of the spine similar to those of juvenile mice. Then the researchers gave the drug to aged mice that have already shown signs of aging, such as muscle loss. After 5 months, the treated mice showed better improvement of treadmill tests than the untreated mice. Their muscle and fat cells do not show signs of aging, although the treatment did not reverse the aging that has already occurred, the team announced today online Nature .
"I think the results are quite striking," said Sharpless. But he warns that further research is needed to understand the effects of the removal of senescent cells. Although they may favor certain disorders related to age, they could prevent other. "Let there be unexpected results of this should be studied further," he said. "Yes, we could do better cataracts, but it will come with the risk of cancer or infections?"
Since the work based on genetically modified mice, it is not directly translatable to humans, said van Deursen. However, researchers can now detect drugs to find compounds that could activate cell death in senescent cells, he said, or could turn the immune system against senescent cells.
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