Medical science may be getting closer to developing better treatments that cause damaged skin in the elderly to repair itself more quickly.
The puzzle may be solved via methods that encourage proteins to speed signals to the body’s immune system to send new skin cells to the wound faster than ever before, Rockefeller University researchers reported in a November issue of Cell.
In wound healing, keratinocytes travel in as a sheet to fill in the wound under a scab. Investigators studied molecular changes in mouse skin, comparing the production of new cells called keratinocytes in 2-month-old versus 24-month old mice, or the rough equivalent to 20- and 70-year-old humans. By enhancing the ability of proteins known as Skints to encourage immune cells to fill in the gaps of healing skin, they noticed an increase in keratinocyte migration to the wound area.
The experiments have shown that with aging, disruptions to communication between skin cells and their immune cells slow down the migration of skin cells that close wounds, said Elaine Fuchs, Ph.D., Rockefeller’s Rebecca C. Lancefield Professor who also leads the Robin Chemers Neustein Laboratory of Mammalian Cell Biology.
She added that study results could point to new approaches to developing treatments to speed elderly wound healing.