Elena Oancea, left, and Nadine Wicks discovered that skin cells contain rhodopsin, a photosensitive receptor used by the eye to detect light. It’s part of human skin’s self-defense against damage to DNA. Image: Mike Cohea/Brown University
most people, tanning seems a simple proposition. A naturally
light-skinned person lies in the sun for hours and ends up as bronzed as
a Jersey Shore star. To scientists, the reaction of skin to ultraviolet
light is more mysterious. A new study demonstrates that skin detects
UVA radiation using a light-sensitive receptor previously found only in
the eye and that this starts melanin production within a couple of
hours. Until now, scientists only knew that melanin production occurred
days after UVB radiation had already begun damaging DNA.
soon as you step out into the sun, your skin knows that it is exposed
to UV radiation,” said senior author Elena Oancea, assistant professor
of biology in the Department of Molecular Pharmacology, Physiology, and
Biotechnology at Brown University. “This is a very fast process, faster
than anything that was known before.”
believe that melanin protects the DNA in skin cells against damage from
UVB rays by absorbing the incoming radiation. It isn’t perfect, which
is why people must use sun block. But the new study in the journal Current Biology shows that the body mounts its defense much sooner, well before it becomes apparent in the form of a tan.
lab experiments with human melanin-producing skin cells called
melanocytes, Oancea, graduate student Nadine Wicks, and their team
discovered that the cells contain rhodopsin, a photosensitive receptor
used by the eye to detect light. Moreover, they traced the steps of how
rhodopsin unleashes calcium ion signals that instigate melanin
Eyes on the skin
the team’s first experiment, the scientists were looking to see whether
UV light instigated a calcium signaling response. They found nothing.
But guessing that the skin might sense light like the eyes do, they
added retinal, a co-factor of opsin receptors including rhodopsin.
“When we did that, we saw an immediate and massive calcium response,” said Wicks, the study’s lead author.
investigations found that the cells contained rhodopsin RNA and
protein. Under UV light, when the scientists reduced rhodopsin levels in
the cells, calcium signaling was reduced. Later, when they starved
cells of retinal, they found that melanin production dropped. The
authors also determined that long-wavelength UVA light, rather than
short-wavelength UVB light, is what stimulates rhodopsin in melanocytes.
A healthy glow
Human melanocyte skin cells fluoresce as their calcium signaling spikes after exposure to ultraviolet light and retinal, a key step in producing melanin. This reaction led researchers to discover the presence of rhodopsin receptors in skin, which detect UVA light.
melanocyte skin cells fluoresce as their calcium signaling spikes after
exposure to ultraviolet light and retinal, a key step in producing
melanin. This led researchers to discover rhodopsin receptors in skin,
which detect UVA light.During several experiments they were able to
trace the following process: When UVA light strikes rhodopsin receptors
with retinal, calcium signals are triggered within a few seconds. After
an hour, measurable amounts of melanin accumulate, although in
relatively small quantities compared to the production that will occur
within 24 hours.
much as they learned, Oancea and Wicks still have some questions. One
is whether rhodopsin is acting alone or in concert with another yet
undiscovered receptor. Another question is whether melanocytes
immediately begin exporting melanin to other kinds of skin cells for
protection or whether they keep the early supply for themselves.
because scientists are learning more about how the skin responds to and
protects itself against UV radiation, Oancea said, that’s no reason for
people to change what they do to protect themselves.
“This doesn’t say, ‘Don’t use sunscreen’,” Oancea said.
In addition to Oancea and Wicks, other authors were Jason Chan, Julia Najera, and Jonathan Ciriello.
University, the National Institutes of Health, and the Natural Sciences
and Engineering Research Council of Canada supported the research.