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. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: J Burn Care Res. 2012 May-Jun;33(3):299–310. doi: 10.1097/BCR.0b013e318240540a

FIGURE 1.

FIGURE 1

Theoretical model for the role of DS in FGF-10 signaling through FGFR2-IIIb in burn wound re-epithelialization [modified from Radek et al., (9)]. (A) In non-burn-injured skin, T cells and fibroblasts reside in the epidermis and dermis, respectively. (B) In keratinocytes, the FGF receptor, FGFR2-IIIb, exists as a monomer on the cell surface. (C) Following burn injury, T cells and fibroblasts secrete FGF-10 into the wound, while small fragments of DS are released into the wound from the extracellular matrix. (D) Enabled by DS, the increase in FGF-10 acts in a paracrine manner through FGFR2-IIIb on keratinocytes. DS promotes receptor dimerization by facilitating the interaction between FGF-10 and FGFR2-IIIb. This interaction ultimately results in downstream signaling that stimulates burn would re-epithelialization by keratinocytes. DS, dermatan sulfate; FGF, fibroblast growth factor; FGFR, fibroblast growth factor receptor.