A membrane protein in skin cells transmits signals that trigger pain and tissue damage that put the 'burn' into sunburn.

Wolfgang Liedtke of Duke University in Durham, North Carolina, and his colleagues switched off production of a cellular ion channel called TRPV4 in the epidermis of genetically engineered mice. They exposed the mice to ultraviolet (UV) radiation, which causes sunburn.

Compared with UV-exposed mice that had normal TRPV4 production, the engineered mice had less damage on their hind-paw pads (which resemble human skin). Their paws were also less sensitive to heat or to being poked with fine wires — signs that the engineered mice experienced less pain. Furthermore, three human patients with sunburn had higher expression of TRPV4 in their epidermis than three unburned controls.

Proc. Natl Acad. Sci. USA http://dx.doi.org/10.1073/pnas.1312933110 (2013)