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(American Journal of Pathology. 2005;166:387-398.)
© 2005 American Society for Investigative Pathology

The Novel Cytokine p43 Stimulates Dermal Fibroblast Proliferation and Wound Repair

Sang Gyu Park^*, Hyosook Shin^*, Young Kee Shin^*, Yeonsook Lee, Eung-Chil Choi^*, Bum-Joon Park^* and Sunghoon Kim^*

From the National Creative Research Initiatives Center for Aminoacyl-tRNA Synthetase (ARS) Network,^* College of Pharmacy, and Imagene Company Biotechnology Incubation Center, Seoul National University, Seoul, Korea

The multifunctional cytokine p43 acts on endothelial and immune cells to control angiogenesis and inflammation. In this report, we describe an additional activity of p43 that specifically promotes fibroblast proliferation and wound repair. In skin wound regions from mice, tumor necrosis factor- induced p43 expression and secretion from macrophages recruited to the site. p43 also promoted fibroblast proliferation through its 146-amino acid N-terminal domain as revealed by deletion mapping. This p43-induced fibroblast proliferation was mediated by extracellular signal-regulated kinase (Erk). Depletion of endogenous p43 in mice by gene disruption retarded wound repair, whereas exogenous supplementation of recombinant human p43 to the wound area stimulated dermal fibroblast proliferation, collagen production, and wound closure. Thus, we have identified a novel p43 activity involving the stimulation of fibroblast proliferation, which could be applied therapeutically to aid wound repair.

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