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. Author manuscript; available in PMC: 2013 Nov 1.
Published in final edited form as: Exp Dermatol. 2012 Aug 9;21(11):822–826. doi: 10.1111/j.1600-0625.2012.01571.x

Figure 1.

Figure 1

Schematic representation of cell types involved in wound healing and the potential effects of S100A8/A9 on those cells. In neutrophils, S100A8/A9 promote expression of inflammatory mediators, phagocytosis, oxidative burst and migration through the epithelium. Likewise, in monocytes, S100A8/A9 stimulate migration and an inflammatory phenotype. Macrophages express and release significantly less S100A8/A9 than do monocytes. Keratinocytes express S100A8/A9 following exposure to inflammatory stimuli, and S100A8/A9 expression results to decreased proliferation, enhanced ROS generation, differentiation and migration as well as increased expression of proinflammatory cytokines and matrixmetalloproteinase-9. When added exogenously, S100A8/A9 promote proliferation of keratinocytes and fibroblasts, which might contribute to the proliferative phase. Thus, S100A8/A9 affect the major cell types involved in wound healing, and these proteins have cell type-selective effects.