Researchers at the UC San Diego School of Medicine announced this week they've discovered that a single molecule might hold the key to curing both psoriasis and slow-healing wounds.
In an article published in Thursday's edition of Immunity, the international team of scientists said they discovered that a molecule called "regenerating islet-derived protein 3-alpha,'' or REG3A is common in skin cells during psoriasis and wound-healing, but not under normal conditions.
Psoriasis is an auto-immune disorder that became infamous with the "heartbreak of psoriasis'' phrase in television commercials.
With psoriasis, skin cells proliferate out of control, causing patches of inflammation and white, scaly skin.
In slow-to-heal wounds, they don't grow fast enough.
"A drug that inhibits the expression of REG3A could represent a more targeted way to treat psoriasis without the systemic immuno-suppression problems of current treatments,'' said Dr. Richard Gallo, a professor of medicine and chief of UCSD's Division of Dermatology. "Conversely, a drug that stimulates or mimics REG3A could boost cell growth and improve wound healing.''
Gallo's team analyzed skin biopsies of patients with and without psoriasis, as well as the skin of mice with psoriasis and wounds on their backs. Blocking REG3A slowed wound-healing but cleared up psoriasis on the mice.
The scientists also found that REG3A acts in concert with an immune system protein involved in a signaling process that prompts skin cells to multiply in excess numbers.
