Source:http://linkedlifedata.com/resource/pubmed/id/21298280
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2011-3-22
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pubmed:abstractText |
Ultraviolet radiation is the major environmental insult to the skin and stimulates the synthesis of melanin in melanocytes, which then distribute it to the neighboring keratinocytes where it confers photo-protection. Skin color results from the paracrine interaction between these two cell types. Recent studies suggest that endocannabinoids are potential mediators in the skin. Here, we investigated whether cannabinoid drugs play a role in melanogenesis and if ultraviolet radiation modifies the cutaneous endocannabinoid system. We used human melanotic melanoma cell line (SK-mel-1) in monoculture or co-culture with human keratinocytes (HaCat). Endocannabinoid levels, cannabinoid receptors expression, and melanin content were evaluated under basal conditions and after ultraviolet-B irradiation (311 nm). We provide evidence that human melanoma cells (SK-mel-1) express CB(1) receptors, and when in co-culture with keratinocytes (HaCat), the selective CB(1) receptor agonist arachidonyl-2-chloroethylamide (ACEA 1 and 10 ?M) inhibited (by 33.4 and 37.3%, respectively) basal melanogenesis. In addition, ultraviolet-B-induced melanogenesis in co-cultures was abolished by ACEA 10 ?M. Both ACEA inhibitory effects were reversed by AM251 (1 ?M), a selective CB(1) antagonist. Furthermore, ultraviolet-B radiation increased endocannabinoids levels only in keratinocytes, whereas CB(1) cannabinoid receptor expression was up-regulated only in melanoma cells. Our results collectively suggest that ultraviolet radiation activates paracrine CB(1)-mediated endocannabinoid signaling to negatively regulate melanin synthesis. The endocannabinoid system in the skin may be a possible target for future therapies in pigmentary disorders.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/AM 251,
http://linkedlifedata.com/resource/pubmed/chemical/Arachidonic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Endocannabinoids,
http://linkedlifedata.com/resource/pubmed/chemical/Melanins,
http://linkedlifedata.com/resource/pubmed/chemical/Piperidines,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Cannabinoid, CB1,
http://linkedlifedata.com/resource/pubmed/chemical/arachidonyl-2-chloroethylamide
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1432-069X
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
303
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
201-10
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pubmed:meshHeading |
pubmed-meshheading:21298280-Arachidonic Acids,
pubmed-meshheading:21298280-Cell Line, Tumor,
pubmed-meshheading:21298280-Coculture Techniques,
pubmed-meshheading:21298280-Down-Regulation,
pubmed-meshheading:21298280-Endocannabinoids,
pubmed-meshheading:21298280-Humans,
pubmed-meshheading:21298280-Keratinocytes,
pubmed-meshheading:21298280-Melanins,
pubmed-meshheading:21298280-Melanocytes,
pubmed-meshheading:21298280-Paracrine Communication,
pubmed-meshheading:21298280-Pigmentation Disorders,
pubmed-meshheading:21298280-Piperidines,
pubmed-meshheading:21298280-Pyrazoles,
pubmed-meshheading:21298280-Receptor, Cannabinoid, CB1,
pubmed-meshheading:21298280-Skin,
pubmed-meshheading:21298280-Ultraviolet Rays
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pubmed:year |
2011
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pubmed:articleTitle |
Inhibition of basal and ultraviolet B-induced melanogenesis by cannabinoid CB(1) receptors: a keratinocyte-dependent effect.
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pubmed:affiliation |
Institute of Pharmacology and Therapeutics, Faculty of Medicine, University of Porto, Portugal. smagina@med.up.pt
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pubmed:publicationType |
Journal Article
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