Last Updated on 10th January 2020 by Caroline Haye
The rather beautiful image above shows human melanocyte cells glowing after exposure to ultraviolet light… Part of an experiment that has, quite literally, shed new light on how our skin produces the melanin that gives it its colour. A research team at Brown University have discovered that a light-sensitive protein related to rhodopsin, is present in skin cells, not just in the eye as previously thought. So, might vitiligo research into rhodopsin could provide a key to possible treatments?
More to tanning than meets the eye
Twenty first century medical science is so advanced and sophisticated – or so we tend to believe – that it comes as a surprise that many of the familiar processes that occur in the human body are still largely a mystery. One process close to my heart, and to the hearts of millions of people around the world living with #vitiligo, is how human skin tans. Almost everyone has a general grasp of how this works: when exposed to sunlight healthy skin creates #melanin – a pigment that darkens the skin in order to protect it from UV damage. Simple, right? Well, maybe not quite so simple after all.
As recently as 2009 scientists began to suspect that the conventional understanding of the tanning mechanism had some significant gaps. A study into Rhodopsin (a light-sensitive protein found in the retina of the eye and responsible for the visual perception of contrast) suggested that a series of such proteins may also be present in skin.
This surprising theory was borne out in 2011 by researchers at Brown University in Providence, Rhode Island, USA. (It seems fitting that research into the tanning process should be carried out at a university called Brown and that Rhodopsin should be studied in Rhode Island… but I digress!) The study found that melanocyte skin cells do indeed detect ultraviolet light using a photosensitive receptor previously thought to exist only in the eye. Not only does skin possess this eye-like ability to sense light, but it triggers melanin production and this melanin production occurs much faster than anyone previously thought. In fact, the initial process starts within seconds of the UV exposure and melanin begins to accumulate within an hour, reaching its peak about 24 hours later.
When I came across these findings online, I immediately wondered if the discovery had prompted any research into how this new knowledge might be used to find a cure for vitiligo. Sadly, I could not find evidence of any such research (although that is not to say that it isn’t ongoing and yet to be published). I also wondered what connection, if any, there might be to the fact that many people with vitiligo have some abnormalities in their retinas (the inner layer of the eye that contains the light-sensitive Rhodopsin cells).
There have been a number of research papers published relating to retinal degeneration in mice with vitiligo. Evidently the Rhodopsin levels in vitiligo mice are lower than in normal mice and the part of the retina in the eye that contains the light receptors is unevenly pigmented. But my very limited grasp of the science involved leaves me unsure of the potential relevance of this to human vitiligo research. So, if anyone reading this post has a better understanding or any insight into the topic, please do get in touch and let me know (Contact Me). I promise to revisit the subject if I find out anything else of interest.
In the meantime, I will content myself with the thought that human skin is even more weird and wonderful than I had previously thought and that, given the sheer number and complexity of processes involved in maintaining its health, it is a wonder that anyone on earth has “normal” skin. In fact, I suspect that we all occupy a position somewhere on the “abnormal” scale to one degree or another and vitiligo is just one example of this reality.
