We’re all too familiar with the symptoms of prolonged exposure to UV rays. There’s the crimson skin, the itchiness, and of course, that overpowering feeling of lethargy. But what actually makes the skin hurt to the touch? A Duke researcher believes he has an answer for sunburned beachgoers: TRPV4.
The protein, which is found in cell membranes in the skin’s outermost layer, begins the pain pathway that culminates in what we feel as sunburn. As ultraviolet B rays meet the skin, they activate TRPV4 molecules, which allow calcium ions to enter the epidermal cells. Close behind the calcium in transit to the epidermis is endothelin, which is both a pain-producing agent and a trigger for the process to start again.
Wolfgang Liedtke, an associate professor of neurology and neurobiology at Duke’s School of Medicine, teamed up with a professor from the University of California in San Francisco and an investigator with the Howard Hughes Medical Institute to design an experiment highlighting TRPV4’s role in producing pain. After genetically engineering mice to lack TRPV4, the researchers exposed the animals’ hind paws to UV-B rays. The mice exhibited little signs of pain or even sensitivity. By comparison, the control group, which did not have their TRPV4 molecules inhibited, yielded the typical effects of sunburn. Liedtke and his colleagues then applied a drug that inhibits TRPV4 to human skin samples, discovering once more that the harmful effects of UV radiation were largely negated.
The findings suggest that TRPV4 inhibitors, if incorporated into the makeup of sunscreen, could alleviate pain resulting from sunburn and perhaps even limit the risk of skin cancer. “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,” says Liedtke.