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Rheumatology Advance Access originally published online on October 1, 2008
Rheumatology 2008 47(12):1754-1760; doi:10.1093/rheumatology/ken370
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Proteomic analysis of scleroderma lesional skin reveals activated wound healing phenotype of epidermal cell layer

N. Aden1, X. Shiwen1, D. Aden1, C. Black1, A. Nuttall1, C. P. Denton1, A. Leask1, D. Abraham1 and R. Stratton1

1Centre for Rheumatology, Royal Free Hospital and University College School of Medicine, London, UK.

Correspondence to: R. Stratton, Centre for Rheumatology, Royal Free Hospital and University College School of Medicine, Royal Free Campus, Rowland Hill Street, London NW3 2QG, UK. E-mail: r.stratton{at}medsch.ucl.ac.uk


  Abstract

Objective. To identify using proteomic analysis, proteins of altered abundance in the skin of patients with SSc.

Methods. 4 mm excision biopsies were obtained from the forearm involved skin of 12 diffuse SSc patients and 12 healthy controls. Two-dimensional gel electrophoresis was used to separate and define proteins in normal and SSc skin biopsy material. Proteins of altered abundance in the disease were formally identified by mass spectroscopy. Abnormalities of the epidermis were confirmed by immunohistochemistry.

Results. Proteomic analysis revealed altered abundance of proteins involved in extracellular matrix production, myofibroblast contractility, energy metabolism and response to oxidative stress. In addition, proteins specific to the epidermis and involved in epidermal cell differentiation were altered in abundance in the disease. SSc epidermis is thickened, has an expanded nucleated cell layer, and exhibits abnormal persistence of basal marker keratin 14, delayed expression of maturation markers keratin 1/10 and the induction of keratins 6 and 16, normally absent from interfollicular skin and induced following epidermal injury. These changes closely resemble the activated phenotype seen during wound healing.

Conclusions. Consistent with previous models of SSc pathogenesis these data are showing increased contractility, increased extracellular matrix and response to oxidative stress in the involved skin of recent onset SSc patients. In addition, we show that SSc epidermis has an activated, wound healing phenotype. These findings are important because epidermal cells activated by injury induce and regulate local fibroblasts during wound repair.

KEY WORDS: Scleroderma, Proteomics, Epidermis, Wound-healing

Submitted 27 April 2008; revised version accepted 12 August 2008.
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