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Aging Longevity Longevity and Age Management

A protein that protects cells from stress can also prolong life, researchers find

10 years, 3 months ago

1728  0
Posted on Feb 20, 2009, 9 a.m. By gary clark

The heat shock response in human cells, which combats exposure to heat, cold and heavy metals, has been found to be regulated by an aging-related protein. This finding suggests that a small amount of stress can actually protect cells from aging.
 

Research conducted by molecular biologist Sandy Westerheide of Northwestern University in Evanston, Illinois and published in the February 20 issue of Science has uncovered evidence that the protein-protecting heat shock response in human cell lines is regulated by Sirtuin 1 (SIRT1), an aging-related protein. This is the first time researchers have found a connection between SIRT1 and the heat shock response. "This is a very interesting and insightful study," notes Raul Mostoslavsky, a cell biologist at the Massachusetts General Hospital Cancer Center and Harvard Medical School in Boston. "We knew that Sirtuin 1 had many roles in longevity. It's remarkable that it also affects heat shock response."

The heat shock response is a natural mechanism found in cells that helps prevent proteins from being damaged as a result of exposure to heat, cold and heavy metals. Such stress can cause proteins to become "unraveled from their usual conformations," leading to cell death. As part of the heat shock response, special protein repair molecules patch damaged proteins and refold them correctly. Cell death is prevented and its life, extended. As study co-author and molecular biologist Richard Morimoto of Northwestern, explains: "A little bit of stress can actually prolong life. Mild stress activates the heat shock response but does not harm the cells."

Researchers still need to prove that the connection between SIRT1 and the heat shock response applies to the protection of cells of whole organisms, not just those cell lines tested by the team. They speculate that sometime in the future, SIRT1 could be used to activate the heat shock response on demand, noting that SIRT1 decreases as the cells age, reducing the heat shock response and minimizing the ability of older cells to cope with damage caused by stress.  "This could help us to age in a more healthy way," Westerheide says. "Heat shock response could also help repair the damaged brain proteins that cause neurodegenerative diseases such as Alzheimer's and Huntington's disease."

News Release: Anti-aging: A little stress may keep cells youthful  www.sciencenews.org February 19, 2009

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