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Human Molecular Genetics Advance Access originally published online on September 23, 2003
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Human Molecular Genetics, 2003, Vol. 12, No. 22 3017-3024
DOI: 10.1093/hmg/ddg320
© 2003 Oxford University Press

Identification of SLURP-1 as an epidermal neuromodulator explains the clinical phenotype of Mal de Meleda

Fabrice Chimienti1, Ronald C. Hogg2, Laure Plantard1, Caroline Lehmann1, Noureddine Brakch3, Judith Fischer4, Marcel Huber1, Daniel Bertrand2 and Daniel Hohl1,*

1Laboratory for Cutaneous Biology, Dermatology Unit, CHUV, Lausanne, Switzerland, 2Department of Physiology, CMU, Geneva, Switzerland, 3Division of Hypertension and Vascular Medicine, CHUV, Lausanne, Switzerland and 4Centre National de Génotypage, Evry, France

Received August 1, 2003; Revised August 21, 2003; Accepted September 11, 2003

Mal de Meleda is an autosomal recessive inflammatory and keratotic palmoplantar skin disorder due to mutations in the ARS B gene, encoding for SLURP-1 (secreted mammalian Ly-6/uPAR-related protein 1). SLURP-1 belongs to the Ly-6/uPAR superfamily of receptor and secreted proteins, which participate in signal transduction, immune cell activation or cellular adhesion. The high degree of structural similarity between SLURP-1 and the three fingers motif of snake neurotoxins and Lynx1 suggests that this protein interacts with the neuronal acetylcholine receptors. We found that SLURP-1 potentiates the human {alpha}7 nicotinic acetylcholine receptors that are present in keratinocytes. These results identify SLURP-1 as a secreted epidermal neuromodulator which is likely to be essential for both epidermal homeostasis and inhibition of TNF-alpha release by macrophages during wound healing. This explains both the hyperproliferative as well as the inflammatory clinical phenotype of Mal de Meleda.

* To whom correspondence should be addressed at: Laboratory for Cutaneous Biology, Dermatology Unit, Beaumont Hospital, CHUV-BT 437, CH-1011 Lausanne, Switzerland. Tel: +41 213140353; Fax: +41 213140382; Email: daniel.hohl{at}hospvd.ch


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