Autophagy linked to beneficial effects of enduring mild stress

Autophagy linked to beneficial effects of enduring mild stress

 

Biologists have known for decades that enduring a short period of mild stress makes simple organisms and human cells better able to survive additional stress later in life. Now, scientists at have found that a cellular process called autophagy is critically involved in providing the benefits of temporary stress. The study, published in Nature Communications, creates new avenues to pursue treatments for neurological disorders such as Huntington's disease.

"We used C. elegans--tiny roundworms used to study fundamental biology--to test the importance of autophagy in becoming stress resistant," says lead author of the study. "They're a great model system because they're transparent, so you can easily observe what goes on inside them, most of their genes and molecular signaling pathways have functional counterparts in humans, and they only live a few weeks, which greatly facilitate measuring their lifespans."

Researchers incubated worms at 36 °C, significantly above the temperature they are usually kept at in the laboratory, for one hour. After this short heat exposure--a mild form of stress that improves the organism's survival--autophagy rates increased throughout the worms' tissues. When they exposed these heat-primed worms to another, longer heat shock a few days later, worms that were deficient in autophagy failed to benefit from the initial mild heat shock, as observed in heat-primed worms with intact autophagy.

Researchers found similar results when they overexpressed heat shock factor -1 (HSF-1) in the worms.

The researchers reasoned that a mild heat stress might also improve the worms' ability to handle another condition that worsens with age--buildup of aggregated proteins, which is stressful for cells. To test this hypothesis, they used worms that model Huntington's disease, a fatal inherited disorder caused by neuronal proteins that start to stick together into big clumps as patients age, leading to degeneration throughout the brain. Exposing worms that make similar sticky proteins in different tissues to a mild heat shock reduced the number of protein aggregates, suggesting that a limited amount of heat stress can reduce toxic protein aggregation.

"Our finding that brief heat exposure helps alleviate protein aggregation is exciting because it could lead to new approaches to slow the advance of neurodegenerative diseases such as Huntington's," says senior author. "The results may also be relevant to Alzheimer's and Parkinson's, which are similarly caused by clumping-prone proteins."

"This research raises many exciting questions," adds the senior author. "For example, how does induction of autophagy by a mild heat stress early on make cells better able to survive heat later--what's the cellular memory? There's a lot to follow up on."

"A lot of people ask us if this means they should start going to the sauna or do hot yoga," jokes lead author. "That may not be an entirely bad idea--epidemiological studies do indicate that frequent sauna use is associated with longer life. But we have a lot more research to do to figure out whether that has anything to do with the beneficial induction of autophagy by heat stress that we see in C. elegans."

http://www.newswise.com/articles/what-doesn-t-kill-you-makes-you-stronger

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