Establishment of a mouse model for post-inflammatory hyperpigmentation.
macrophage
melanin
melanocyte
mouse model
pigmentation
Journal
Pigment cell & melanoma research
ISSN: 1755-148X
Titre abrégé: Pigment Cell Melanoma Res
Pays: England
ID NLM: 101318927
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
21
05
2020
accepted:
23
06
2020
pubmed:
6
7
2020
medline:
24
11
2021
entrez:
6
7
2020
Statut:
ppublish
Résumé
Post-inflammatory hyperpigmentation (PIH) is a common cutaneous condition that can cause a disfigured appearance. However, the pathophysiology of PIH remains poorly understood, at least in part, because an appropriate animal model for research has not been established. In order to analyze the pathomechanism of PIH, we successfully induced PIH in a hairless version of transgenic mice (hk14-SCF Tg/HRM) that have a human-type epidermis containing melanin by repeated hapten application of 2,4-dinitrofluorobenzene. Histopathologic observation showed epidermal hyperplasia, predominant infiltrations of inflammatory cells, and melanin-containing cells in the dermis just after elicitation of the atopic dermatitis-like condition. At week 2, the findings were similar to the characteristics of PIH, that is, an increase of melanin without spongiosis or liquid degeneration in the epidermis and an increase in dermal melanophages. Dynamic analysis of melanin showed that the melanin in the dermis remained for a longer duration than in the epidermis. Furthermore, immunohistochemical staining revealed that the majority of cells containing melanin were positive for the anti-CD68 antibody, but negative for the anti-F4/80 antibody. These data suggest that novel treatments of PIH should be targeted against macrophages and should eventually lead to the development of new treatment modalities.
Substances chimiques
Melanins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101-110Informations de copyright
© 2020 John Wiley & Sons A/S . Published by John Wiley & Sons Ltd.
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