The Expression of the alpha-Melanocyte Stimulating Hormone (alpha-MSH) and Melanocortin-1 Receptor (MC1R) in the Epidermis of the Vitiligo / 대한피부과학회지
Korean Journal of Dermatology
;
: 690-695, 2003.
Article
Dans Coréen
| WPRIM
| ID: wpr-160813
ABSTRACT
BACKGROUND:
Vitiligo is a skin disease that is characterized by the loss of cutaneous pigmentation. alpha-Melanocyte stimulating hormone (alpha-MSH) is a neuroimmunomodulating peptide derived from proopiomelanocortin, and melanocortin-1 receptor (MC1R) is a surface receptor which is expressed by several other cutaneous cells including melanocyte and keratinocyte. Both of them have been known to be the main physiologic regulator for integumental pigmentation.OBJECTIVE:
To evaluate the expression pattern of alpha-MSH and MC1R in the epidermis of vitiligo patients.METHODS:
Specimens were obtained in lesional, perilesional and non-lesional skin in 10 patients with vitiligo and from 3 normal persons by the punch biopsy. And then, indirect immunofluorescence was done to show the pattern of expression of alpha-MSH and MC1R.RESULTS:
Pattern of expression between alpha-MSH and MC1R was nearly the same. In vitiligo patients with stable disease state (7 of 10), the expression of alpha-MSH and MC1R in the non-lesional skin was more prominent than that in lesional area. In vitiligo patients with active disease state (3 of 10), the expression of alpha-MSH and MC1R in the lesional skin was more prominent than that in non-lesional area.CONCLUSION:
Between the stable and active vitiligo patients, there was a different pattern of expression of alpha-MSH and MC1R in the lesional skin.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Peau
/
Maladies de la peau
/
Vitiligo
/
Biopsie
/
Pro-opiomélanocortine
/
Pigmentation
/
Hormone mélanotrope alpha
/
Kératinocytes
/
Technique d'immunofluorescence indirecte
/
Récepteur de la mélanocortine de type 1
Limites du sujet:
Humains
langue:
Coréen
Texte intégral:
Korean Journal of Dermatology
Année:
2003
Type:
Article
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