August 6, 2013
By Blocking A Molecule In Our Skin, Sunburn Pain May Become A Thing Of The Past
Susan Bowen for redOrbit.com - Your Universe Online
According to new research, we could have a future free of sunburn pain. A new study shows how we have a molecule in our epidermis that creates our bodies' reaction to sun exposure. The molecule is called TRPV4, and by blocking this molecule, researchers were able to protect skin from the pain of sunburn. The study was published in the Proceedings of the National Academy of Sciences.It might also be helpful in mitigating other types of pain. "We have uncovered a novel explanation for why sunburn hurts," said Wolfgang Liedtke, MD, PhD, one of the senior authors of the study and associate professor of neurology and neurobiology at Duke University School of Medicine. "If we understand sunburn better, we can understand pain better because what plagues my patients day in and day out is what temporarily affects otherwise healthy people who suffer from sunburn."
Most sunburns are caused by UVB radiation. A moderate amount of sunlight is good for the body, producing Vitamin D. Just a little too much though, and it damages the DNA in skin cells and could lead to cancer. The pain of sunburn is skin's signal it is past time to get out of the sun.
TRPV4 is a molecule found abundantly in skin and is known to be involved in other pain processes. It is an ion channel, that is, a gateway in the cell membrane that quickly lets in positively charged ions, such as calcium and sodium. The researchers wanted to determine if it also played a role in the pain and tissue damage caused by UVB exposure.
The team conducted their experiments on mice and human skin samples. The mice they used were genetically engineered not to have TRPV4 in the cells of the epidermis. For these mice and the normal control mice the team exposed the hind paws to UVB rays. The hind paws more closely resemble human skin. The skin of the normal mice blistered after the exposure, but the mutant mice showed little damage.
They next step used a device engineered by Dr. Nan Marie Jokerst, a professor of electrical and computer engineering at Duke's engineering school. Using the device, they showed UVB caused calcium to flow into skin cells, but only when the TRPV4 ion channel was present. This event alerts another molecule, called endothelin, which tells the TRPV4 to send in even more calcium. Endothelin is known to cause pain and itching.
They repeated the process using human skin samples and got the same results.
To see if they could block this pain pathway, the researchers used a pharmaceutical compound called GSK205 that selectively inhibits TRPV4. Mixing it with alcohol and glycerol, they applied it to the cultured cells of normal mice and found it was effective in blocking the incoming calcium ions.
"The results position TRPV4 as a new target for preventing and treating sunburn, and probably chronic sun damage including skin cancer or skin photo-aging, though more work must be done before TRPV4 inhibitors can become part of the sun defense arsenal, perhaps in new kinds of skin cream, or to treat chronic sun damage," said Dr. Martin Steinhoff, co-senior author of the study.
It will be important to determine whether or not TRPV4 blockers affect other processes going on in the skin. Perhaps in the future it will be added to traditional sunscreen to provide even stronger sun protection.