| Keratinocyte dysfunction in vitiligo epidermis: cytokine microenvironment and correlation to keratinocyte apoptosis. | |
MedLine Citation:
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PMID: 19475531 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
Authors:
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Silvia Moretti; Paolo Fabbri; Gianna Baroni; Samantha Berti; Daniele Bani; Emilio Berti; Romina Nassini; Torello Lotti; Daniela Massi |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Histology and histopathology Volume: 24 ISSN: 1699-5848 ISO Abbreviation: Histol. Histopathol. Publication Date: 2009 Jul |
Date Detail:
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Created Date: 2009-05-28 Completed Date: 2009-08-19 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8609357 Medline TA: Histol Histopathol Country: Spain |
Other Details:
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Languages: eng Pagination: 849-57 Citation Subset: IM |
Affiliation:
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Department of Dermatological Sciences, University of Florence, Florence, Italy. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Apoptosis* Biopsy Case-Control Studies Child Child, Preschool Cytokines / metabolism* Epidermis / metabolism*, ultrastructure Female Fluorescein-5-isothiocyanate / metabolism Fluorescent Dyes / metabolism Humans Immunohistochemistry In Situ Hybridization, Fluorescence In Situ Nick-End Labeling Infant Keratinocytes* / chemistry, metabolism, pathology, ultrastructure Male Melanocytes / physiology RNA, Messenger / metabolism Vitiligo / metabolism*, surgery Young Adult |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Fluorescent Dyes; 0/RNA, Messenger; 3326-32-7/Fluorescein-5-isothiocyanate |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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