The regenerative capacity of skin starts declining with age, but the exact mechanism of why this happens is still unknown. Researchers from Japan have recently identified a mechanism to explain why this happens and potentially how it can be fixed.
The study results were published in the Journal of Cell Biology. Researchers from Tokyo Medical and Dental University have revealed that the ability of skin stem cells to repair skin after an injury may be linked with their ability to move towards the site of injury.
The researchers demonstrated a link between epidermal growth factor receptor (EGFR) signaling and type XVII collagen proteolysis on age-associated alteration on age-associated alteration of keratinocyte stem cell dynamics in skin regeneration.
Skin stem cells are called keratinocyte stem cells and are responsible for skin regeneration and wound closure through a process called re-epithelialization.
The study team compared the wound healing and proliferative ability of skin stem cells derived from young mice and aged mice. They evaluated how EGFR drives skin stem cell motility and that EGFR signalling is reduced in old stem cells. EGFR acts by preventing the degradation of a specific type of collagen, COL17A1, which is necessary to hold the layers of the skin together.
COL17A1 coordinates the movement of skin stem cells towards the injury by regulating actin and keratin filaments networks in the cells. he researchers found that with age, a decrease in EGFR signalling occurs, leading to lower levels of COL17A1 and skin stem cells with reduced mobility that are less able to re-epithelialize the skin.
They concluded that EGFR-COL17A1 axis-mediated keratinocyte stem cell motility drives epidermal regeneration, which provides a novel therapeutic approach for age-related impaired skin regeneration.
Tokyo Medical and Dental University. “Skin stem cells get moving for enhanced skin regeneration.” ScienceDaily. ScienceDaily, 15 October 2021.
Daisuke Nanba, et al. EGFR-mediated epidermal stem cell motility drives skin regeneration through COL17A1 proteolysis. Journal of Cell Biology, 2021; 220 (11) DOI: 10.1083/jcb.202012073