Human wound healing typically results in a scar, or fibrous tissue that replaces normal skin. A University of Pennsylvania-led team has found an unlikely factor that could change this process and minimize scarring: hair follicles.
Human scar tissue contains excess collagen and is devoid of hair follicles and cutaneous fat. But the team found that active hair follicles can drive the formation of fat cells. In the study, published in Science, they noticed that adult mice sometimes regenerated hair follicles near a wound site. Clustered around these new follicles were new fat cells that were indistinguishable from normal fat cells.
They confirmed their suspicions when they put skin cells from a wound into a culture that stimulates fat cell differentiation. Myofibroblasts—cells that can speed wound healing—only converted to fat cells in the presence of hair follicles.
It turned out that actively growing hair follicles produced proteins called Bmp2 and Bmp4, which encourage the reprogramming of myofibroblasts into fat cells. Deleting a BMP receptor in mice blocked the formation of new fat cells even in the presence of hair follicles, while exposing myofibroblasts to BMP promoted their conversion into fat cells.
“The findings support a window of opportunity after wounding to influence the regeneration rather than scarring of tissue by activating embryonic pathways and converting myofibroblasts to adipocytes,” the researchers wrote in the study. “Our work shows that hair follicles grow independently of fat and that hair follicle regeneration is necessary and proximal to cutaneous fat regeneration.” BMP signaling may be a promising target for regenerating hair follicles in patients with disorders lacking fat, such as acute scars, keloids, lipodystrophies and aging, they said.
Skin isn’t the only organ that scars. Scarring, or fibrosis, is a major component of multiple chronic diseases, such as Crohn’s disease and cirrhosis. St. Louis University scientists are working on a drug to fight pancreatic fibrosis by blocking a protein called transforming growth factor beta, while University of British Columbia researchers have discovered a genetic mutation that protects mice from intestinal scarring similar to that found in Crohn’s patients.