Researchers Decode Sunburn, Find Possible Treatment

In a new study,scientists have found that increased levels of a single molecule called TRPV4 is responsible for sunburns.

Researchers also found that blocking this key molecule using a pharmaceutical compound could help make the burns less painful.

Sunlight helps the body produce vitamin D and maintains the circadian rhythm. However, exposure to a lot of ultraviolet B or UVB radiation could lead to sunburns which are nature's way of telling the body that it is receiving more sun exposure than needed.

Sunburn symptoms might be temporary, but the skin damage is usually permanent, according to Medline Plus. Sunburns increase risk of premature aging and skin cancers. In some people, severe blistering can cause death also.

"We have uncovered a novel explanation for why sunburn hurts. 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," said said Wolfgang Liedtke, M.D., associate professor of neurology and neurobiology at Duke University School of Medicine and one of the senior authors of the study.

The study was conducted on a group of mouse models and human skin samples. Researchers tested the role of TRPV4 in developing sunburns. TRPV4 is an ion-channel that lets positively charged ions such as calcium and sodium into the skin. The molecule is known to regulate pain.

For the study, researchers first knocked-out the gene that codes the molecules in a set of mice. The genetically engineered mice and normal mice were then exposed to UVB radiations. Specifically, researchers exposed the hind paws of the animals to the radiations as it resembles human skin.

Researchers found that hind paws of control animals (the one with TRPV4) developed blisters while the genetically altered mice showed no effects.

The mouse cells were then cultured to analyze the effects of TRPV4. Researchers found that in the presence of TRPV4, calcium ions readily flow into the skin.

Researchers uncovered the following mechanism that leads to sunburn:  UVB radiations activate TRPV4, which leads to influx of calcium ions in the skin. The presence of calcium ions in abundance leads to the release of endothelin, which is known to cause pain and itching.

They even found that a pharmaceutical compound called GSK205 could effectively reduce the risk of sunburns in mice models.

The study included Elaine Fuchs, Ph.D., a professor at Rockefeller University and Martin Steinhoff, M.D., Ph.D., professor of dermatology and surgery at the University of California.

"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 Steinhoff, co-senior author of the study.

The study is published in the journal Proceedings of the National Academy of Sciences (PNAS).