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Molecular Relationship between Endocannabinoid System and Disease 2.0
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Molecular Relationship between Endocannabinoid System and Disease 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 15159

Special Issue Editor

Prof. Dr. Chiara Laezza

E-Mail Website
Guest Editor
Institute of Endocrinology and Experimental Oncology, IEOS CNR, Via Pansini 5, 80131 Naples, Italy
Interests: mevalonate pathway; prenylation proteins; cannabinoid and cancer; cell cycle; cancer-related biochemical pathways; cell proliferation; cell signaling; breast cancer; glioblastoma multiforme
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The endocannabinoid system (ECS) is a biological system involved in the regulation of multiple pathophysiological processes. Alterations of ECS expression and activity have been described in many pathological conditions, including cancers and neurological disorders. Therefore, its pharmaceutical modulation has attracted considerable attention as a target for the development of novel therapeutics. This Special Issue focuses on the molecular relationships between the ECS and diseases including cancers as well as neurological, metabolic, and autoimmune pathologies, with emphasis on recent breakthroughs in the field. The aim of this Special Issue is to encourage studies on the therapeutic potential of cannabinoids in preclinical studies and their possible use in the treatment of the diseases mentioned above. Authors are invited to submit high-quality original research articles and reviews contributing to the knowledge on the role of the endocannabinoid system in the pathological processes.

Prof. Dr. Chiara Laezza
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

  • cannabinoids
  • endocannabinoids
  • endocannabinoid system
  • neurological diseases
  • metabolic disorders
  • autoimmune diseases
  • cancer progression

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Related Special Issue

Published Papers (5 papers)

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Research

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14 pages, 2714 KiB  
Article
Omega-3 Recovers Cannabinoid 1 Receptor Expression in the Adult Mouse Brain after Adolescent Binge Drinking
by Ane Martín-Llorente, Maitane Serrano, Itziar Bonilla-Del Río, Leire Lekunberri, Garazi Ocerin, Nagore Puente, Almudena Ramos, Irantzu Rico-Barrio, Inmaculada Gerrikagoitia and Pedro Grandes
Int. J. Mol. Sci. 2023, 24(24), 17316; https://doi.org/10.3390/ijms242417316 - 10 Dec 2023
Cited by 1 | Viewed by 1890
Abstract
Adolescent binge drinking is a social problem with a long-lasting impact on cognitive functions. The cannabinoid type-1 (CB1) receptor of the endocannabinoid system (ECS) is involved in brain synaptic plasticity, cognition and behavior via receptor localization at specific subcellular compartments of [...] Read more.
Adolescent binge drinking is a social problem with a long-lasting impact on cognitive functions. The cannabinoid type-1 (CB1) receptor of the endocannabinoid system (ECS) is involved in brain synaptic plasticity, cognition and behavior via receptor localization at specific subcellular compartments of the cortical, limbic and motor regions. Alcohol (EtOH) intake affects the ECS, CB1 and their functions. Evidence indicates that binge drinking during adolescence impairs memory via the abrogation of CB1-dependent synaptic plasticity in the hippocampus. However, the impact of EtOH consumption on global CB1 receptor expression in the adult brain is unknown. We studied this using optical density analysis throughout brain regions processed for light microscopy (LM) immunohistotochemistry. CB1 staining decreased significantly in the secondary motor cortex, cerebellum, cingulate cortex, amygdala and nucleus accumbens. Next, as omega-3 (n-3) polyunsaturated fatty acids (PUFAs) rescue synaptic plasticity and improve EtOH-impaired cognition, we investigated whether docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) had any effect on CB1 receptors. N-3 intake during EtOH abstinence restored CB1 immunostaining in the secondary motor cortex, cerebellum and amygdala, and ameliorated receptor density in the cingulate cortex. These results show that n-3 supplementation recovers CB1 receptor expression disrupted by EtOH in distinct brain regions involved in motor functions and cognition. Full article
(This article belongs to the Special Issue Molecular Relationship between Endocannabinoid System and Disease 2.0)
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27 pages, 4659 KiB  
Article
Oleoylethanolamide Treatment Modulates Both Neuroinflammation and Microgliosis, and Prevents Massive Leukocyte Infiltration to the Cerebellum in a Mouse Model of Neuronal Degeneration
by Ester Pérez-Martín, Laura Pérez-Revuelta, Cristina Barahona-López, David Pérez-Boyero, José R. Alonso, David Díaz and Eduardo Weruaga
Int. J. Mol. Sci. 2023, 24(11), 9691; https://doi.org/10.3390/ijms24119691 - 2 Jun 2023
Cited by 4 | Viewed by 3518
Abstract
Neurodegenerative diseases involve an exacerbated neuroinflammatory response led by microglia that triggers cytokine storm and leukocyte infiltration into the brain. PPARα agonists partially dampen this neuroinflammation in some models of brain insult, but neuronal loss was not the triggering cause in any of [...] Read more.
Neurodegenerative diseases involve an exacerbated neuroinflammatory response led by microglia that triggers cytokine storm and leukocyte infiltration into the brain. PPARα agonists partially dampen this neuroinflammation in some models of brain insult, but neuronal loss was not the triggering cause in any of them. This study examines the anti-inflammatory and immunomodulatory properties of the PPARα agonist oleoylethanolamide (OEA) in the Purkinje Cell Degeneration (PCD) mouse, which exhibits striking neuroinflammation caused by aggressive loss of cerebellar Purkinje neurons. Using real-time quantitative polymerase chain reaction and immunostaining, we quantified changes in pro- and anti-inflammatory markers, microglial density and marker-based phenotype, and overall leukocyte recruitment at different time points after OEA administration. OEA was found to modulate cerebellar neuroinflammation by increasing the gene expression of proinflammatory mediators at the onset of neurodegeneration and decreasing it over time. OEA also enhanced the expression of anti-inflammatory and neuroprotective factors and the Pparα gene. Regarding microgliosis, OEA reduced microglial density—especially in regions where it is preferentially located in PCD mice—and shifted the microglial phenotype towards an anti-inflammatory state. Finally, OEA prevented massive leukocyte infiltration into the cerebellum. Overall, our findings suggest that OEA may change the environment to protect neurons from degeneration caused by exacerbated inflammation. Full article
(This article belongs to the Special Issue Molecular Relationship between Endocannabinoid System and Disease 2.0)
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15 pages, 2502 KiB  
Article
The Cannabinoid Ligand Arachidonyl-2′-Chloroethylamide (ACEA) Ameliorates Depressive and Overactive Bladder Symptoms in a Corticosterone-Induced Female Wistar Rat Model
by Łukasz Zapała, Grzegorz Niemczyk, Piotr Zapała, Artur Wdowiak, Iwona Bojar, Tomasz Kluz, Aleksandra Szopa, Anna Serefko, Piotr Radziszewski and Andrzej Wróbel
Int. J. Mol. Sci. 2023, 24(4), 3820; https://doi.org/10.3390/ijms24043820 - 14 Feb 2023
Cited by 3 | Viewed by 2203
Abstract
There is growing need to increase the knowledge on the cannabinoid ligands in the treatment of overactive bladder. Among potential candidates, arachidonyl-2′-chloroethylamide (ACEA), a selective cannabinoid CB1 receptor agonist is proposed. The aim of this paper was to determine if ACEA, a selective [...] Read more.
There is growing need to increase the knowledge on the cannabinoid ligands in the treatment of overactive bladder. Among potential candidates, arachidonyl-2′-chloroethylamide (ACEA), a selective cannabinoid CB1 receptor agonist is proposed. The aim of this paper was to determine if ACEA, a selective cannabinoid CB1 receptor agonist, could reverse the effects of corticosterone (CORT), characteristic of depressive and bladder overactivity potential. The animals (48 female rats) were divided into four groups: I—control, II—received CORT, III—received ACEA, and IV—received the combination of CORT and ACEA. The conscious cystometry, forced swim test (FST), and locomotor activity measurements were performed 3 days after the last dose of ACEA, followed by ELISA measurements. In group IV, ACEA restored urodynamic parameters that were altered by CORT. CORT prolonged the immobility time in FST and the values were lowered by ACEA. ACEA normalized the expression of c-Fos in all the analyzed central micturition centers (group IV vs. group II). ACEA restored the CORT-induced changes in the biomarkers in urine (BDNF, NGF), bladder detrusor (VAChT, Rho kinase), bladder urothelium (CGRP, ATP, CRF, OCT-3, TRPV1), and hippocampus (TNF-α, IL-1β and Il-6, CRF, IL-10, BDNF, NGF). In conclusion, ACEA was proven to reverse CORT-induced changes in both cystometric and biochemical parameters that are determinants of OAB/depression, which represents an example of an existing link between OAB and depression via cannabinoid receptors. Full article
(This article belongs to the Special Issue Molecular Relationship between Endocannabinoid System and Disease 2.0)
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Review

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17 pages, 530 KiB  
Review
Neuroprotection and Beyond: The Central Role of CB1 and CB2 Receptors in Stroke Recovery
by Bashir Bietar, Sophie Tanner and Christian Lehmann
Int. J. Mol. Sci. 2023, 24(23), 16728; https://doi.org/10.3390/ijms242316728 - 24 Nov 2023
Cited by 9 | Viewed by 4341
Abstract
The endocannabinoid system, with its intricate presence in numerous cells, tissues, and organs, offers a compelling avenue for therapeutic interventions. Central to this system are the cannabinoid receptors 1 and 2 (CB1R and CB2R), whose ubiquity can introduce complexities in targeted treatments due [...] Read more.
The endocannabinoid system, with its intricate presence in numerous cells, tissues, and organs, offers a compelling avenue for therapeutic interventions. Central to this system are the cannabinoid receptors 1 and 2 (CB1R and CB2R), whose ubiquity can introduce complexities in targeted treatments due to their wide-ranging physiological influence. Injuries to the central nervous system (CNS), including strokes and traumatic brain injuries, induce localized pro-inflammatory immune responses, termed neuroinflammation. Research has shown that compensatory immunodepression usually follows, and these mechanisms might influence immunity, potentially affecting infection risks in patients. As traditional preventive treatments like antibiotics face challenges, the exploration of immunomodulatory therapies offers a promising alternative. This review delves into the potential neuroprotective roles of the cannabinoid receptors: CB1R’s involvement in mitigating excitotoxicity and CB2R’s dual role in promoting cell survival and anti-inflammatory responses. However, the potential of cannabinoids to reduce neuroinflammation must be weighed against the risk of exacerbating immunodepression. Though the endocannabinoid system promises numerous therapeutic benefits, understanding its multifaceted signaling mechanisms and outcomes remains a challenge. Full article
(This article belongs to the Special Issue Molecular Relationship between Endocannabinoid System and Disease 2.0)
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22 pages, 2224 KiB  
Review
The Implications of Cannabinoid-Induced Metabolic Dysregulation for Cellular Differentiation and Growth
by Tina Podinić, Geoff Werstuck and Sandeep Raha
Int. J. Mol. Sci. 2023, 24(13), 11003; https://doi.org/10.3390/ijms241311003 - 2 Jul 2023
Cited by 6 | Viewed by 2491
Abstract
The endocannabinoid system (ECS) governs and coordinates several physiological processes through an integrated signaling network, which is responsible for inducing appropriate intracellular metabolic signaling cascades in response to (endo)cannabinoid stimulation. This intricate cellular system ensures the proper functioning of the immune, reproductive, and [...] Read more.
The endocannabinoid system (ECS) governs and coordinates several physiological processes through an integrated signaling network, which is responsible for inducing appropriate intracellular metabolic signaling cascades in response to (endo)cannabinoid stimulation. This intricate cellular system ensures the proper functioning of the immune, reproductive, and nervous systems and is involved in the regulation of appetite, memory, metabolism, and development. Cannabinoid receptors have been observed on both cellular and mitochondrial membranes in several tissues and are stimulated by various classes of cannabinoids, rendering the ECS highly versatile. In the context of growth and development, emerging evidence suggests a crucial role for the ECS in cellular growth and differentiation. Indeed, cannabinoids have the potential to disrupt key energy-sensing metabolic signaling pathways requiring mitochondrial-ER crosstalk, whose functioning is essential for successful cellular growth and differentiation. This review aims to explore the extent of cannabinoid-induced cellular dysregulation and its implications for cellular differentiation. Full article
(This article belongs to the Special Issue Molecular Relationship between Endocannabinoid System and Disease 2.0)
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