Using a small interfering RNA to block the action of the NaX sodium sensor in the skin appears to prevent the triggering of inflammation in wounds, allowing them to heal faster and with less scarring, according to findings published in Science Translational Medicine (Nov. 4, 2015; 7(312):312ra177).
The researchers write that the sensor triggers the production of mediators of epithelial cell proliferation and inflammation that may lead to scar formation. Both scar formation and atopic-dermatitis-like symptoms in animal models were decreased when NaX was blocked, according to the paper.
“This is a really novel pathway we identified. Nobody has ever tried to develop a product that gets at this pathway before,” lead author Wei Xu, PhD., assistant professor at the Louisiana State University AgCenter and the School of Renewable Natural Resources in Baton Rouge, said in a press release.
According to the release, the discovery of NaX’s role in wound healing was built upon prior research by Xu’s post-doctoral research adviser, Dr. Thomas Mustoe. Dr. Mustoe had shown that areas of skin with high hydration heal faster. This, and the fact that human skin holds much more sodium ions than other ions, led Xu and his team to suspect a key role for the body’s sodium regulators in wound healing.
Xu and his colleagues developed a nanoparticle to deliver the interfering RNA, which can be applied to the skin in a cream or lotion.
“I think this is going to be very promising in skin disease treatments,” Xu said in the release. “If we target the very beginning of the pathway, we can control the expression levels of the inflammation factors.”