Inhibition of basal and ultraviolet B-induced melanogenesis by cannabinoid CB1 receptors: a keratinocyte-dependent effect

• Tipo: Artigo em Revista Científica Internacional
• Data: 2011

Autores

magina, s (Autor) FMUP; esteves-pinto, c (Autor) Outra; moura, e (Autor) Outra; serrao, mp (Autor) Outra; moura, d (Autor) FMUP; petrosino, s (Autor) Outra; di marzo, v (Autor) Outra; vieira-coelho, ma (Autor) FMUP

Revista

Título: Archives of Dermatological Research

Vol. 303

Páginas: 201-210

ISSN: 0340-3696

Editora: Springer Nature

Indexação

ISI Web of Knowledge - 28 Citações

Scopus - 31 Citações

Classificação Científica

FOS: Ciências médicas e da saúde > Medicina clínica

Outras Informações

ID Authenticus: P-002-SWN

DOI: 10.1007/s00403-011-1126-z

Abstract (EN): 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 CB1 receptors, and when in co-culture with keratinocytes (HaCat), the selective CB1 receptor agonist arachidonyl-2-chloroethylamide (ACEA 1 and 10 mu 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 mu M. Both ACEA inhibitory effects were reversed by AM251 (1 mu M), a selective CB1 antagonist. Furthermore, ultraviolet-B radiation increased endocannabinoids levels only in keratinocytes, whereas CB1 cannabinoid receptor expression was up-regulated only in melanoma cells. Our results collectively suggest that ultraviolet radiation activates paracrine CB1-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.

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 10