Expression of SKALP/elafin during wound healing in human skin
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Skin-derived antileukoproteinase (SKALP), also known as elafin, is a proteinase inhibitor with specificity for polymorphonuclear leucocyte (PMN)-derived elastase and proteinase-3. SKALP is absent in normal human epidermis, but is strongly induced in inflammatory dermatoses such as psoriasis. SKALP is putatively involved in the regulation of cutaneous inflammation by inhibiting PMN derived proteinases. The aim of this study was to investigate SKALP expression and PMN infiltration during wound healing in human skin. This was examined in healing excisional wounds in normal skin and in impaired healing in various types of chronic venous ulcers. Tissues were analysed using immunohistochemistry and Northern blot analysis. Healing of excisional wounds was studied from day 0 to day 14. An influx of PMN was seen rapidly after wounding and was maximal between day 2 and 4 and then subsided. SKALP was induced within 48 h and was expressed in the suprabasal keratinocytes of the wound edge and the migrating epidermal sheet. SKALP expression was maximal on day 4 and was downregulated at the time of complete reepithelialization (7–14 days). In venous ulcers, PMN were abundant in the wound bed and scarce under the wound edge. SKALP was strongly expressed in the keratinocytes of the wound edge in all types of ulcers studied. In the wound bed, SKALP was not detectable. Our results suggest that SKALP plays a role in the acute, inflammatory phase of wound healing. From the kinetics and topology of SKALP expression we surmise that it negatively regulates PMN infiltration.
Key wordsSKALP Wound healing Antileukoproteinase Elastase
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- 5.Chang A, Schalkwijk J, Happle R, Kerkhof PC van de (1990) Elastase-inhibiting activity in scaling skin disorders. Acta Derm Venereol (Stockh) 70:147–151Google Scholar
- 6.Reference deletedGoogle Scholar
- 7.Clark RAF (1993) Mechanisms of cutaneous wound repair. In: Westerhof W (ed) Leg ulcers: diagnosis and treatment. Elsevier Science, Amsterdam, pp 29–50Google Scholar
- 14.Saheki T, Ito F, Hagiwara H, Saito Y, Kuroki J, Tachibana S, Hirose S (1992) Primary structure of the human elafin precursor preproelafin deduced from the nucleotide sequence of its gene and the presence of unique repetitive sequences in the prosegment. Biochem Biophys Res Commun 185:240–245PubMedCrossRefGoogle Scholar
- 16.Sallenave J, Schullmann J, Crosley J, Jordana M, Gauldie J (1995) Regulation of secretory leukocyte proteinase inhibitor (SLPI) and elastase-specific inhibitor (ESI/elafin) in human airway epithelial cells by cytokines and neutrophilic enzymes. Am J Resp Cell Mol biol 11:733–741Google Scholar
- 17.Reference deletedGoogle Scholar
- 21.Tonnesen MG, Worthen GS, Johnston RB (1988) Neutrophil emigration, activation, and tissue damage. In: Clark RAF, Henson PM (eds) Molecular and cellular biology of wound repair. Plenum Press, New York, pp 149–183Google Scholar