S100A8 accelerates wound healing by promoting adipose stem cell proliferation and suppressing inflammation.

Abstract

Adipose-derived stem cells (ADSCs) are stem cells with multidirectional differentiation potential isolated from adipose tissue. They have the same immunomodulatory effect as bone marrow mesenchymal stem cells in wound repair and immune regulation as bone marrow. The mechanism of action of ADSCs in skin wound repair has not been elucidated. S100A8 is a calcium and zinc binding protein, but its role in skin wound healing is rarely reported. We herein show that S100A8 overexpression significantly promoted ADSC proliferation and differentiation, whereas S100A8 knockdown yielded the opposite results. A skin injury model with bone exposure was created in rats by surgically removing the skin from the head and exposing the skull. The wounds were treated with S100A8-overexpressing or S100A8-knockdown ADSCs, and wound healing was monitored. The serum levels of the inflammation-related factors tumor necrosis factor-α and interleukin-6 were decreased significantly after S100A8 overexpression, while the angiogenic factor vascular endothelial growth factor and connective tissue generating factor showed the opposite trend. Histological staining revealed that granulation tissue neovascularization was more pronounced in wounds treated with S100A8-overexpressing ADSCs than that in the control group. We conclude that S100A8 promotes the proliferation of ADSCs and inhibits inflammation to improve skin wound healing.