Document Detail

Ultraviolet B radiation-stimulated urocortin 1 is involved in tyrosinase-related protein 1 production in human melanoma HMV-II cells.
MedLine Citation:
PMID:  25240771     Owner:  NLM     Status:  Publisher    
Ultraviolet B (UVB) radiation stimulates cutaneous melanin pigmentation. The melanosomal enzyme tyrosinase-related protein 1 (TRP1) is involved in the modulation of pigment production in response to this stressor. Recent molecular and biochemical analyses have revealed the presence of corticotropin-releasing factor (CRF) and urocortin 1 (Ucn1), together with their corresponding receptors, in mammalian skin. Although CRF and Ucn1 are thought to have potent effects on the skin system, their possible roles and regulations have yet to be determined fully. Our previous findings in human melanoma HMV-II cells suggest that both CRF and Ucn1 regulate TRP1 gene expression via Nurr-1/Nur77, transcription factors that constitute the nuclear receptor 4a subgroup of orphan nuclear receptors. HMV-II cells were found to express mainly Ucn1 mRNA. This study aimed to explore the effects of UVB on Ucn1 mRNA and TRP1 protein levels in HMV-II cells. UVB (30mJ/cm(2)) increased Nurr-1, Nur77, and Ucn1 mRNA levels. UVB also increased TRP1 protein levels. Ucn1 knockdown inhibited the UVB-induced increases in TRP1 protein levels. These data suggest that UVB-stimulated Ucn1 contributes to TRP1 production via the transcription of both Nurr-1 and Nur77. Ucn1, produced in melanoma cells, acts on melanoma cells themselves in an autocrine manner.
Yutaka Watanuki; Kazunori Kageyama; Shinobu Takayasu; Yasushi Matsuzaki; Yasumasa Iwasaki; Makoto Daimon
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-9-18
Journal Detail:
Title:  Peptides     Volume:  -     ISSN:  1873-5169     ISO Abbreviation:  Peptides     Publication Date:  2014 Sep 
Date Detail:
Created Date:  2014-9-22     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8008690     Medline TA:  Peptides     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014. Published by Elsevier Inc.
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