Endocannabinoids Stimulate Human Melanogenesis via Type-1 Cannabinoid Receptor

Pucci, Mariangela; Pasquariello, Nicoletta; Battista, Natalia; Tommaso, Morena Di; Rapino, Cinzia; Fezza, Filomena; Zuccolo, Michela; Jourdain, Roland; Agró, Alessandro Finazzi; Breton, Lionel; Maccarrone, Mauro

doi:10.1074/jbc.m111.314880

Cited by 66 publications

(58 citation statements)

References 73 publications

(107 reference statements)

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“…or physiological saline, and decapitated 1 h, 6 h, 12 h or 24 h after the treatment. Brains were removed and the striata were dissected on ice and frozen on dry ice, then tissues were subjected to lipid extraction with chloroform/ methanol (2:1, v/v), in the presence of d 8 -AEA and d 8 -2-AG as internal standards (Pucci et al, 2012). The organic phase was dried and then analyzed by liquid chromatography-electrospray ionization mass spectrometry (LCeESI-MS), using a single quadrupole API-150EX mass spectrometer (Applied Biosystem, CA, USA) in conjunction with a PerkinElmer LC system (PerkinElmer, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

“…The organic phase was dried and then analyzed by liquid chromatography-electrospray ionization mass spectrometry (LCeESI-MS), using a single quadrupole API-150EX mass spectrometer (Applied Biosystem, CA, USA) in conjunction with a PerkinElmer LC system (PerkinElmer, MA, USA). Quantitative analysis was performed by selected ion recording over the respective sodiated molecular ions, as reported (Pucci et al, 2012). …”

Section: Methodsmentioning

confidence: 99%

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Prior stimulation of the endocannabinoid system prevents methamphetamine-induced dopaminergic neurotoxicity in the striatum through activation of CB2 receptors

et al. 2014

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Methamphetamine toxicity is associated with cell death and loss of dopamine neuron terminals in the striatum similar to what is found in some neurodegenerative diseases. Conversely, the endocannabinoid system (ECS) has been suggested to be neuroprotective in the brain, and new pharmacological tools have been developed to increase their endogenous tone. In this study, we evaluated whether ECS stimulation could reduce the neurotoxicity of high doses of methamphetamine on the dopamine system. We found that methamphetamine alters the levels of the major endocannabinoids, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) in the striatum, suggesting that the ECS participates in the brain responses to methamphetamine. Δ9-tetrahydrocannabinol (THC), a cannabis-derived agonist of both CB1 and CB2 cannabinoid receptors, or inhibitors of the main enzymes responsible for the degradation of AEA and 2-AG (URB597 and JZL184, respectively), blunted the decrease in striatal protein levels of tyrosine hydroxylase induced by methamphetamine. In addition, antagonists of CB2, but not of CB1, blocked the preventive effects of URB597 and JZL184, suggesting that only the former receptor subtype is engaged in neuroprotection exerted by ECS stimulation. Finally, we found that methamphetamine increases striatal levels of the cytokine tumor necrosis factor alpha, an effect that was blocked by ECS stimulation. Altogether, our results indicate that stimulation of ECS prior to the administration of an overdose of meth-amphetamine considerably reduces the neurotoxicity of the drug through CB2 receptor activation and highlight a protective function for the ECS against the toxicity induced by drugs and other external insults to the brain. This article is part of the Special Issue entitled ‘CNS Stimulants’.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Prior stimulation of the endocannabinoid system prevents methamphetamine-induced dopaminergic neurotoxicity in the striatum through activation of CB2 receptors

et al. 2014

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“…In the epidermis, AEA inhibits proliferation and reduces differentiation of human epidermal keratinocytes via CB1-coupled signaling (697). CB1 controls melanogenesis in epidermal melanocytes too (696), possibly also through intercellular communication mechanisms involving the keratinocytes (516). Interestingly, in mice, genetic ablation of CB1 delays, whereas lack of CB2 accelerates, recovery of the epidermal permeability barrier, which is keratinocyte proliferation and differentiation dependent (738).…”

Section: Skinmentioning

confidence: 99%

From Phytocannabinoids to Cannabinoid Receptors and Endocannabinoids: Pleiotropic Physiological and Pathological Roles Through Complex Pharmacology

Ligresti¹,

Petrocellis²,

Marzo³

2016

Physiological Reviews

377

337

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Apart from having been used and misused for at least four millennia for, among others, recreational and medicinal purposes, the cannabis plant and its most peculiar chemical components, the plant cannabinoids (phytocannabinoids), have the merit to have led humanity to discover one of the most intriguing and pleiotropic endogenous signaling systems, the endocannabinoid system (ECS). This review article aims to describe and critically discuss, in the most comprehensive possible manner, the multifaceted aspects of 1) the pharmacology and potential impact on mammalian physiology of all major phytocannabinoids, and not only of the most famous one ⌬ 9 -tetrahydrocannabinol, and 2) the adaptive prohomeostatic physiological, or maladaptive pathological, roles of the ECS in mammalian cells, tissues, and organs. In doing so, we have respected the chronological order of the milestones of the millennial route from medicinal/recreational cannabis to the ECS and beyond, as it is now clear that some of the early steps in this long path, which were originally neglected, are becoming important again. The emerging picture is rather complex, but still supports the belief that more important discoveries on human physiology, and new therapies, might come in the future from new knowledge in this field.

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“…(ii) TRPV1 is co-localized with CB1 and CB2 in cerebromicrovascular endothelial cells [62] and with CB1 in endothelial cells from mesenteric arteries of cirrhotic rats [63,64]; (iii) TRPV1 is co-localized with both CB1 and CB2 in mouse bone-marrowderived dendritic cells [65], and in human skeletal muscle cells [66], myometrial smooth muscle cells [67], osteoclasts [68], proximal tubular (HK2) cells of the kidney [69], keratinocytes [70,71], melanocytes [72] and dental pulp cells [73]; (iv) TRPV1 is co-localized only with CB1 in human sperm cells [74], and only with CB2 in synoviocytes from rats after intraarticular injection of mono-iodo-acetate, a model of osteoarthritis [75]. In view of the previously reported cross-talk between TRPV1 and CB1 receptors at the level of down-stream signalling events [76,77], these many examples of co-expression between the channel and one or both cannabinoid receptor sub-types offer the opportunity of widening further the range of pharmacological effects that endogenous mediators capable of activating both types of receptors may have, and, hence, the extent of 'plasticity' that their action can produce in a large variety of biological systems.…”

Section: Co-expression Of Cb1 or Cb2 Receptors And Trpv1 Channels In mentioning

confidence: 99%

Why do cannabinoid receptors have more than one endogenous ligand?

Marzo

Petrocellis

2012

Phil. Trans. R. Soc. B

252

176

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The endocannabinoid system was revealed following the understanding of the mechanism of action of marijuana's major psychotropic principle, D 9-tetrahydrocannabinol, and includes two G-proteincoupled receptors (GPCRs; the cannabinoid CB1 and CB2 receptors), their endogenous ligands (the endocannabinoids, the best studied of which are anandamide and 2-arachidonoylglycerol (2-AG)), and the proteins that regulate the levels and activity of these receptors and ligands. However, other minor lipid metabolites different from, but chemically similar to, anandamide and 2-AG have also been suggested to act as endocannabinoids. Thus, unlike most other GPCRs, cannabinoid receptors appear to have more than one endogenous agonist, and it has been often wondered what could be the physiological meaning of this peculiarity. In 1999, it was proposed that anandamide might also activate other targets, and in particular the transient receptor potential of vanilloid type-1 (TRPV1) channels. Over the last decade, this interaction has been shown to occur both in peripheral tissues and brain, during both physiological and pathological conditions. TRPV1 channels can be activated also by another less abundant endocannabinoid, N-arachidonoyldopamine, but not by 2-AG, and have been proposed by some authors to act as ionotropic endocannabinoid receptors. This article will discuss the latest discoveries on this subject, and discuss, among others, how anandamide and 2-AG differential actions at TRPV1 and cannabinoid receptors contribute to making this signalling system a versatile tool available to organisms to fine-tune homeostasis.

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Endocannabinoids Stimulate Human Melanogenesis via Type-1 Cannabinoid Receptor

Cited by 66 publications

References 73 publications

Prior stimulation of the endocannabinoid system prevents methamphetamine-induced dopaminergic neurotoxicity in the striatum through activation of CB2 receptors

Prior stimulation of the endocannabinoid system prevents methamphetamine-induced dopaminergic neurotoxicity in the striatum through activation of CB2 receptors

From Phytocannabinoids to Cannabinoid Receptors and Endocannabinoids: Pleiotropic Physiological and Pathological Roles Through Complex Pharmacology

Why do cannabinoid receptors have more than one endogenous ligand?

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