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

• Type: Article in International Scientific Journal
• Date: 2011

Authors

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

Journal

Title: Archives of Dermatological Research

Vol. 303

Pages: 201-210

ISSN: 0340-3696

Publisher: Springer Nature

Indexing

ISI Web of Knowledge - 26 Citations

Scopus - 28 Citations

Scientific classification

FOS: Medical and Health sciences > Clinical medicine

Other information

Authenticus ID: 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.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 10