Washington: Back from a beach holiday with an unwelcome souvenir: a painful, red sunburn?

In a breakthrough, scientists have found a potential new way to soothe sunburn pain and redness.

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 has found.

Blocking this molecule, called TRPV4, greatly protects against the painful effects of sunburn, researchers said.

The research 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 Wolfgang Liedtke, one of the senior authors of the study from the Duke University School of Medicine.

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.

First, they built a mouse model that was missing TRPV4 only in cells of the epidermis, the outermost layer of skin.

They took these genetically engineered mice and their normal counterparts and exposed their hind paws – which most resemble human skin – to UVB rays.

The hind paws of the normal mice became hypersensitive and blistered in response to the UVB exposure, while those of the mutant mice showed little sensitisation and tissue injury.

Next, they used cultured mouse skin cells to dissect the activities of TRPV4.

To test whether these findings in mice and mouse cells have human relevance, researchers used human skin samples to successfully demonstrate increased activation of TRPV4 and endothelin which is known to cause pain in humans and also evokes itching, in human epidermis after UVB exposure.

They used a pharmaceutical compound called GSK205 that selectively inhibits TRPV4.

They dissolved this compound into a solution of alcohol and glycerol – basically, skin disinfectant – and then applied it to the hind paws of normal mice.

The researchers found that the mice treated with the compound were again 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 defence arsenal, perhaps in new kinds of skin cream, or to treat chronic sun damage,” said Martin Steinhoff, from the University of California in San Francisco.

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