Fight Aging! Newsletter, June 6th 2016

This study teaches us that poor wound healing and wrinkling and sagging that occur in aging skin share similar mechanisms."

Reduced cell cohesiveness of outgrowths from eccrine sweat glands delays wound closure in elderly skin

Human skin heals more slowly in aged vs. young adults, but the mechanism for this delay is unclear. In humans, eccrine sweat glands (ESGs) and hair follicles underlying wounds generate cohesive keratinocyte outgrowths that expand to form the new epidermis. Our results confirm that the outgrowth of cells from ESGs is a major feature of repair in young skin. Strikingly, in aged skin, although ESG density is unaltered, less than 50% of the ESGs generate epithelial outgrowths during repair (vs. 100% in young). Surprisingly, aging does not alter the wound-induced proliferation response in hair follicles or ESGs. Instead, there is an overall reduced cohesiveness of keratinocytes in aged skin. Reduced cell-cell cohesiveness was most obvious in ESG-derived outgrowths that, when present, were surrounded by unconnected cells in the scab overlaying aged wounds.

Failure to form cohesive ESG outgrowths may reflect impaired interactions of keratinocytes with the damaged extracellular matrix (ECM) in aged skin. Previous work from our group and others has characterized in detail the age-associated damage to the skin dermal ECM, which includes increased collagen fiber fragmentation, reduced ECM resistance, and decreased tissue mechanical force....

Source: Fight Aging! - June 5, 2016 Category: Research Authors: Reason Tags: Newsletters Source Type: blogs