Researchers from Brown University in Rhode Island studied the reaction of melanocytes to UV light and found that an ion channel well-known elsewhere in the body for its chemical sensitivity, plays a central role in the process of protecting the skin.
Identifying ion channel
Last year, university researchers discovered that certain skin cells use a light-sensitive receptor found outside of the eye to sense ultraviolet light and quickly begin pumping out melanin to protect against DNA damage.
The new discovery, published in the Proceedings of the National Academy of Sciences, is that human melanocyte skin cells rely on an ion channel called TRPA1 to allow a flood of calcium ions into the cells when they are exposed to UVA light.
The resulting abundance of calcium ions signals the cell to begin making melanin, the pigment responsible for the tanning response in people, and this new finding could be a target in the future for products looking to improve this protective response.
As a matter of basic science, the finding strengthens the evidence of a striking parallel between the skin's response to UVA light and the way the eye detects light.
"It's exciting because it confirms this phototransduction pathway is similar to those found in the eye. It consists of a light-sensitive receptor, molecular signaling cascade, and an ion channel," says Elena Oancea, assistant professor of medical science at Brown.
"The involvement of an ion channel makes this pathway a lot more like other phototransduction pathways."
Oancea and lead author Nicholas Bellono say that the chemical sensitivity of TRPA1 offers the intriguing possibility that it could become a target for experiments to boost melanin production.
They emphasized, however, that people who go out in the sun should always take widely recommended precautions to protect their skin, such as using high-SPF commercial sunscreens.
To begin with the team sought to identify the TRP ion channel responsible for the UVA-activation in melanocytes, as this was not clear before.
The team hit on TRPA1 after several experiments and amassed considerable evidence to confirm its vital role.
In one experiment, they treated melanocytes with "antagonist" chemicals known to block TRPA1 activity, finding that melanocytes produce little or no melanin following exposure to UVA when TRPA1 is blocked.
They did not, however, do experiments to see whether adding TRPA1 stimulating substances could increase melanin production.