Doctors have found a way to manipulate wounds to heal as regenerated skin rather than scar tissue. The method involves transforming the most common type of cells found in wounds into fat cells – something that was previously thought to be impossible in humans. Researchers began this work at the Perelman School of Medicine at the University of Pennsylvania, which led to a large-scale, multi-year study in connection with the Plikus Laboratory for Developmental and Regenerative Biology at the University of California, Irvine. They published their findings online in the journal Science on Thursday, January 5th, 2017.
Fat cells called adipocytes are normally found in the skin, but they’re lost when wounds heal as scars. The most common cells found in healing wounds are myofibroblasts, which were thought to only form a scar. Scar tissue also does not have any hair follicles associated with it, which is another factor that gives it an abnormal appearance from the rest of the skin. Researchers used these characteristics as the basis for their work – changing the already present myofibroblasts into fat cells that do not cause scarring.
“Essentially, we can manipulate wound healing so that it leads to skin regeneration rather than scarring,” said George Cotsarelis, MD, the chair of the Department of Dermatology and the Milton Bixler Hartzell Professor of Dermatology at Penn, and the principal investigator of the project. “The secret is to regenerate hair follicles first. After that, the fat will regenerate in response to the signals from those follicles.”
The study showed hair and fat develop separately but not independently. Hair follicles form first, and the Cotsarelis lab previously discovered factors necessary for their formation. Now they’ve discovered additional factors actually produced by the regenerating hair follicle to convert the surrounding myofibroblasts to regenerate as fat instead of forming a scar. That fat will not form without the new hairs, but once it does, the new cells are indistinguishable from the pre-existing fat cells, giving the healed wound a natural look instead of leaving a scar.
As they examined the question of what was sending the signal from the hair to the fat cells, researchers identified a factor called Bone Morphogenetic Protein (BMP). It instructs the myofibroblasts to become fat. This signaling was groundbreaking on its own, as it changed what was previously known about myofibroblasts.
“Typically, myofibroblasts were thought to be incapable of becoming a different type of cell,” Cotsarelis said. “But our work shows we have the ability to influence these cells, and that they can be efficiently and stably converted into adipocytes.” This was shown in both the mouse and in human keloid cells grown in culture.
… These discoveries have the potential to be revolutionary in the field of dermatology. The first and most obvious use would be to develop a therapy that signals myofibroblasts to convert into adipocytes – helping wounds heal without scarring.
… But the increase of fat cells in tissue can also be helpful for more than just wounds. Adipocyte loss is a common complication of other conditions… The cells are also lost naturally because of the aging process, especially in the face, which leads to permanent, deep wrinkles, something anti-aging treatments can’t fix in a cosmetically satisfactory way.
“Our findings can potentially move us toward a new strategy to regenerate adipocytes in wrinkled skin, which could lead us to brand new anti-aging treatments,” Cotsarelis said. …
Until we can go in for skin regeneration treatments, there is vitamin C.
Marcus S. Cooke and G. Don Jones found that a form of Vitamin C helped to promote wound healing and also helped protect the DNA damage of skin cells.
Previously, the group has published evidence that DNA repair is upregulated in people consuming vitamin C supplements. The researchers have now provided some mechanistic evidence for this, in cell culture, using techniques such as Affymetrix microarray, for looking at gene expression, and the ‘Comet’ assay to study DNA damage and repair.
Duarte said, “The exposure to solar ultraviolet radiation increases in summer, often resulting in a higher incidence of skin lesions. Ultraviolet radiation is also a genotoxic agent responsible for skin cancer, through the formation of free radicals and DNA damage.
“Our study analysed the effect of sustained exposure to a vitamin C derivative, ascorbic acid 2-phosphate (AA2P), in human dermal fibroblasts. We investigated which genes are activated by vitamin C in these cells, which are responsible for skin regeneration.
“The results demonstrated that vitamin C may improve wound healing by stimulating quiescent fibroblasts to divide and by promoting their migration into the wounded area. Vitamin C could also protect the skin by increasing the capacity of fibroblasts to repair potentially mutagenic DNA lesions.”