Document Detail

Keratinocyte dysfunction in vitiligo epidermis: cytokine microenvironment and correlation to keratinocyte apoptosis.
MedLine Citation:
PMID:  19475531     Owner:  NLM     Status:  MEDLINE    
Vitiligo is a skin disorder characterized by loss of functional melanocytes. Keratinocytes contribute to melanocyte homeostasis, and keratinocyte alteration may play a role in melanocyte dysfunction in vitiligo. In particular, the release of melanogenic mediators and the level of functioning keratinocytes may affect melanocyte dysfunction in vitiligo epidermis. Keratinocyte-derived mediators involved in pigmentation, analysed by in situ hybridization, and epidermal apoptosis, detected by TUNEL assay and electron microscopy, were evaluated in lesional and perilesional skin biopsies from 15 patients with active vitiligo and in 5 control subjects. Among the melanogenic mediators, stem cell factor (SCF) and endothelin-1 (ET-1) mRNA were significantly reduced in lesional as compared to perilesional epidermis, whereas no difference was observed in mRNA of basic fibroblastic growth factor (bFGF) and granulocyte-monocyte colony stimulating factor (GM-CSF). The expression of mRNA for tumor necrosis factor (TNF)-alpha and interleukin-6 (IL-6), two pro-inflammatory cytokines with an inhibitory effect on pigmentation, was increased in the epidermis from vitiligo biopsies, whereas their expression was practically undetectable in the skin of control subjects. Apoptotic keratinocytes were more abundant in lesional vs. perilesional skin of vitiligo patients and were absent in the epidermis of control subjects. Changes in expression of keratinocyte-derived mediators observed in the present study are consistent with their differential functions in melanocyte regulation. In particular, increased TNF-alpha could contribute to keratinocyte apoptosis, which results in reduced release of melanogenic cytokines and ultimately in melanocyte disappearance.
Silvia Moretti; Paolo Fabbri; Gianna Baroni; Samantha Berti; Daniele Bani; Emilio Berti; Romina Nassini; Torello Lotti; Daniela Massi
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Histology and histopathology     Volume:  24     ISSN:  1699-5848     ISO Abbreviation:  Histol. Histopathol.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-05-28     Completed Date:  2009-08-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8609357     Medline TA:  Histol Histopathol     Country:  Spain    
Other Details:
Languages:  eng     Pagination:  849-57     Citation Subset:  IM    
Department of Dermatological Sciences, University of Florence, Florence, Italy.
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MeSH Terms
Case-Control Studies
Child, Preschool
Cytokines / metabolism*
Epidermis / metabolism*,  ultrastructure
Fluorescein-5-isothiocyanate / metabolism
Fluorescent Dyes / metabolism
In Situ Hybridization, Fluorescence
In Situ Nick-End Labeling
Keratinocytes* / chemistry,  metabolism,  pathology,  ultrastructure
Melanocytes / physiology
RNA, Messenger / metabolism
Vitiligo / metabolism*,  surgery
Young Adult
Reg. No./Substance:
0/Cytokines; 0/Fluorescent Dyes; 0/RNA, Messenger; 3326-32-7/Fluorescein-5-isothiocyanate

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