Beauty may be only skin deep, but for scientists working at the scale of single molecules, it can go deeper still. A joint research team from UC Davis and Peking University has shown for the first time how the active ingredient in cosmetic treatments such as facial peels function at the molecular level to produce the exfoliation effect by which newer, fresher skin cells are exposed.
In a paper published in the Journal of Biological Chemistry, the authors report that glycolic acid, a common ingredient in topical anti-wrinkle creams, causes skin cells to die by activating a specific ion-channel protein – a complex molecule which regulates the passage of electrically charged molecules into and out of the cell membrane – allowing an influx of calcium.
“Calcium is a very important ion for life because calcium is a signal ion used in biology in many, many ways,” said Dr. Jie Zheng, professor of physiology and membrane biology at the UC Davis School of Medicine and a co-author of the study. “But if we let a lot of calcium into the cell, the intracellular signaling gets totally screwed up and the cell will die.”
Glycolic acid is part of a family of molecules known as alpha hydroxyl acids (AHAs). Until now it was thought that AHAs worked by loosening the bonds between already dead cells and the underlying live tissue, rather than killing the cells with the help of a protein sensitive to the acidification caused by AHA molecules diffusing into the cell’s interior.
This protein, called TRPV3, is part of a family of proteins that have been studied for their ability to act as heat and pain sensors, helping to maintain a constant body temperature and regulate our physiological reactions to “hot” foods such as chilis. In what Zheng described as “a total surprise,” TRPV3 was found to be highly expressed in the skin.
“The channel was first discovered in sensory neurons, and it was discovered as a heat sensor,” Zheng said. “Later on people realized that actually this channel is expressed in the skin a lot, and people started to wonder, ‘Why is it there?’”
The “why” is still an open question, since the role of TRPV3 under normal physiological conditions remains unclear. However, a major part of the “how” of TRPV3’s role in exfoliation has been established for the first time.
Zheng jokes that this process wasn’t evolved for the purpose of making us look prettier. Instead, he says, “we found by accident a way to use this process [in cosmetics] without realizing it.”
However, with a greater understanding of the mechanisms involved, it may be possible to mitigate side effects such as itching and inflammation.
“I think the [cosmetics] industry was doing this wrong,” said Zheng. “We use a very strong dose of acid, of course we get rid of the old skin on the surface. But what happens after that? What we need to do is find ways to promote that process without hurting the good cells underneath. So I think if the industry realized that, and finds ways to do that, we may have some much better products.”
Zheng says he doesn’t know to what extent anyone in the cosmetics industry is taking notice. For his part, the more interesting questions surround the function of TRPV3 in human health. For example, a genetic mutation in TRPV3 results in a skin disorder known as Olmsted syndrome, characterized by mutilated patches of skin and whose symptoms include severe itching.
“What is probably as important, if not more important, is to know whether we can use [this knowledge] to cure disease or treat conditions to improve human life. Those are things that are arguably more important. And of course to me as a scientist, it is just as interesting to simply understand how nature works.”
OYANG TENG can be reached at email@example.com.