THE EXPRESSION OF THE C-KIT - RECEPTOR BY EPIDERMAL MELANOCYTES MAY BE REDUCED IN VITILIGO

Citation
A. Norris et al., THE EXPRESSION OF THE C-KIT - RECEPTOR BY EPIDERMAL MELANOCYTES MAY BE REDUCED IN VITILIGO, British journal of dermatology, 134(2), 1996, pp. 299-306
Citations number
26
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
00070963
Volume
134
Issue
2
Year of publication
1996
Pages
299 - 306
Database
ISI
SICI code
0007-0963(1996)134:2<299:TEOTC->2.0.ZU;2-O
Abstract
The proto-oncogene c-kit encodes the transmembrane tyrosine kinase rec eptor that has a role in the growth regulation of various cell types i ncluding melanocytes. In the present study we have examined the expres sion of the c-kit protein in the skin of seven patients with vitiligo, Melanocytes positive for c-kit protein were observed in the basal lay er in non-lesional skin and the mean number of 25.8 +/- 5.2 (per 200 b asal cells) compared with that of 21.8 +/- 3.5 from six control subjec ts. In perilesional skin there was a reduction in the numbers of c-kit positive melanocytes (6.7 +/- 2.6) and this was especially noticeable in six of the seven patients. Such a reduction was less obvious follo wing staining with MEL-5 and in only two subjects were the numbers of melanocytes below the normal range. This suggests that the reduction i n c-kit staining was the result of decreased expression of the protein rather than a loss of melanocytes. No melanocytes, positive for c-kit protein, or after staining with MEL-5, were identified in lesional sk in although isolated tyrosinase-positive melanocytes were seen in one subject. There was no apparent change in the numbers of mast cells exp ressing c-kit protein and the intensity of staining in the dermis even in lesional skin was similar to that in the controls. These results d emonstrate that c-kit protein is present on melanocytes in adult human skin and that in perilesional skin of some vitiligo patients there is a reduction in the numbers of melanocytes expressing this receptor, W hether this may contribute to the defective melanocyte growth and/or s urvival that occurs in vitiligo or whether it is a consequence of mela nocyte damage remains to be seen.