NOV-DEC 2018

MedEsthetics—business education for medical practitioners—provides the latest noninvasive cosmetic procedures, treatment trends, product and equipment reviews, legal issues and medical aesthetics industry news.

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64 NOVEMBER/DECEMBER 2018 | MedEsthetics NEWSMAKERS | By Inga Hansen In the aesthetics industry, the focus is typically on how to make aging skin behave more like younger skin. But a new discovery suggests that, in the case of wound healing, help- ing young skin behave more like older skin may reduce scar formation and improve tissue regeneration. "Dermatologists and plastic surgeons have consistently observed that older people's wounds heal with thinner scars than younger patients', but until now, no one has been able to answer the question of why that's the case," says Thomas H. Leung, MD, PhD, assistant professor of dermatology at the Perelman School of Medicine, Univer- sity of Pennsylvania. For their study, ""Aging Suppresses Skin-Derived Circulat- ing SDF1 to Promote Full-Thickness Tissue Regeneration" (Cell Reports, September 25, 2018), Dr. Leung and his colleagues pierced the ears of one-month and 18-month- old mice—the equivalent of a 12-year-old and a 70-year-old if converted to human years. The holes closed with no scar formation in older mice, while younger mice healed with visible scars. Similarly, when they performed full-thickness excisional wounding assays on the back skin of young and older mice, the wounds in the young mice healed with fi brotic scars. The back wounds on the older mice healed with minor scars and a return of the hair follicles. When the researchers exchanged the blood of young mice with old mice and pierced their ears, they found that the ears of the older mice now scarred. Hypothesizing that whatever was causing the scarring must be something in the blood, the team took tissue samples from young and old mice and compared their gene expression signatures. They identifi ed 80 differences then narrowed the list down to only those gene products found in the bloodstream. Among the 13 genetic differences, one stood out: stromal cell-derived factor 1 (SDF1), a signaling molecule previously shown to play a role in scar formation in the skin, liver and lungs. To determine whether SDF1 may be the causal factor, they created a mouse that lacked SDF1 in the skin. When SDF1 function was inactivated, even young mice began to regenerate skin like the older mice. The team then grew human skin in the lab and injured it with a scalpel. "Similar to the mouse, wounded young human skin contained higher levels of SDF1 transcript compared with wounded aged human skin," says Dr. Leung. The researchers note that young skin does heal faster than older skin, but more imperfectly. They posit that from an evolutionary perspective fast and imperfect healing may have been favored over slow and perfect tissue regenera- tion. "This is a rare instance where aging actually improves the body's ability to heal rather than diminishing it," says Dr. Leung. "When we're younger, we secrete more SDF1 into the blood stream to form scars, but as we age, we lose this ability, which allows tissue to regenerate." The research team next plans to study the use of SDF1 inhibitors—currently used as a treatment to mobilize stem cells—for scar prevention in humans. Inga Hansen is the executive editor of MedEsthetics. Stromal cell-derived factor 1 may hold the key to scarless wound healing. SDF1 AND SCAR FORMATION Thomas H. Leung, MD, PhD "When we're younger, we secrete more SDF1 into the blood stream to form scars, but as we age, we lose this ability, which allows tissue to regenerate."

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