Here - EWMA 2013

P 222
POSTER PRESENTATIONS
Poster: Basic Science
POSTER: BASIC SCIENCE
P 223
SUBCUTANEOUS ADIPOCYTES IN WOUND HEALING
– THE ROLE OF ADIPONECTIN
Poster: Basic Science
Revital Mandil Levin 1 , M. Ben-Hamou 1 , L. Braiman-Wiksman 1
1 HealOr Ltd. (Rechovot, Israel).
Growing body of evidence demonstrates that adipocytes affect skin physiology and
response to injury. However, a direct functional association between subcutaneous fat
and skin cells has not been established.
We have shown that in full thickness incisional wounds, subcutaneous adipocytes are
recruited to the wound gap as early as 4 days post wounding and associated with
keratinocyte migration and closure. We have also demonstrated that subcutaneous fat
supernatants and homogenates enhanced healing progression by secretion of biological
active proteins. In diabetes, subcutaneous adipocytes display abnormal morphology
which was correlated with wound healing impairments. In order to identify the mediator
responsible for the healing effects of adipocytes, we screened various adipokines for
their ability to induce wound healing in vitro. Our screening suggested adiponectin to
specifically induce epidermal keratinocytes and fibroblasts migration mediated by
adiponectin receptors AdipoR1/R2. In vivo, adiponectin expression is induced at the
wound site surrounding newly recruited adipocytes. However, in diabetic wounds,
adiponectin secretion was significantly reduced. Finally, treatment of animal wounds with
adiponectin significantly improved all wound healing parameters including epidermal
closure (67% vs. 33%), dermal closure (83% vs. 50%) and reduced inflammation (17%
vs. 83%). These adiponectin-induced effects are mediated through the activation of
insulin signalling cascade without affecting AMPK activation. In conclusion, impaired
wound healing as it appears in diabetes is associated with defective subcutaneous
adipocytes distribution and reduced adiponectin secretion suggesting a causative role for
adiponectin and adipocytes in wound healing impairment and as a potential therapeutic
for the treatment of diabetic ulcers.
WITHDRAWN
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