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Discovery Could Lead to End of Sunburn Pain
Researchers find potential treatment for chronic sun damage, including skin cancer (August 5)
The painful, red skin that comes from too much time in the sun is caused by a molecule abundant in the skin’s epidermis, a new study shows.
Blocking this molecule, called TRPV4, greatly protects against the painful effects of sunburn. The results were published online in the Proceedings of the National Academy of Sciences. The research, which was conducted in mouse models and human skin samples, could yield a way to combat sunburn and possibly several other causes of pain.
“We have uncovered a novel explanation for why sunburn hurts,” said senior author Wolfgang Liedtke, MD, PhD, associate professor of neurology and neurobiology at Duke University School of Medicine. “If we understand sunburn better, we can understand pain better because what plagues my patients day in and day out is what temporarily affects otherwise healthy people who suffer from sunburn.”
Most sunburns are caused by ultraviolet B (UVB) radiation. In moderation, this component of sunlight does the body good, giving a daily dose of vitamin D and perhaps improving mood. But if people get too much, it can damage the DNA in their skin cells and increase their susceptibility to cancer. Sunburns are nature’s way of telling people to go inside and avoid further damage.
The researchers investigated whether the TRPV4 molecule, which is abundant in skin cells and has been shown to be involved in other pain processes, might play a role in the pain and tissue damage caused by UVB over-exposure. TRPV4 is an ion channel — a gateway in the cell membrane that rapidly lets in positively charged ions, such as calcium and sodium.
To see whether they could block this pain pathway, the researchers used a pharmaceutical compound called GSK205 that selectively inhibits TRPV4. They found that mice treated with the compound were largely resistant to the pain-inducing and skin-disrupting effects of sunburn. Similarly, when they administered the compound to mouse skin cells in culture, they found that it stopped the UV-triggered influx of calcium ions into the cells.
“The results position TRPV4 as a new target for preventing and treating sunburn, and probably chronic sun damage, including skin cancer or skin photo-aging, though more work must be done before TRPV4 inhibitors can become part of the sun defense arsenal, perhaps in new kinds of skin cream, or to treat chronic sun damage,” said co-senior author Martin Steinhoff, MD, PhD.
Source: Duke University; August 5, 2013.