Anti-inflammatory effects of N-acylethanolamines in rheumatoid arthritis synovial cells are mediated by TRPV1 and TRPA1 in a COX-2 dependent manner

Lowin, Torsten; Apitz, Martin; Anders, Sven; Straub, Rainer H.

doi:10.1186/s13075-015-0845-5

Cited by 81 publications

(56 citation statements)

References 36 publications

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“…A possible anti‐inflammatory mechanism involves the down‐regulation of MAPK signalling by AEA. Activation of the endocannabinoid system can be beneficial in arthritis, and manipulating this system (especially by using a combination of COX‐2 and a FAAH inhibitor) might be a promising strategy to reduce erosions and inflammation in arthritis (Lowin et al ., ). This emphasizes the importance of elucidating the involvement of the endocannabinoid signalling in OA in further detail.…”

Section: Cannabinoids In Synovial Tissuementioning

confidence: 97%

Joint problems arising from lack of repair mechanisms: can cannabinoids help?

Małek

Starowicz

2018

British J Pharmacology

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Osteoarthritis (OA) is the most common disease of joints, which are complex organs where cartilage, bone and synovium cooperate to allow a range of movements. During progression of the disease, the function of all three main components is jeopardized. Nevertheless, the involvement of each tissue in OA development is still not established and is the topic of the present review. The OA therapies available are symptomatic, largely targeting pain management rather than disease progression. The strong need to develop a treatment for cartilage degeneration, bone deformation and synovial inflammation has led to research on the involvement of the endocannabinoid system in the development of OA. The current review discusses the research on this topic to date and notes the advantages of exploiting endocannabinoid system modulation for cartilage, bone and synovium homeostasis, which could prevent the further progression of OA.

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Section: Cannabinoids In Synovial Tissuementioning

confidence: 97%

Joint problems arising from lack of repair mechanisms: can cannabinoids help?

Małek

Starowicz

2018

British J Pharmacology

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“…Interestingly, TRP channels also play a role in rheumatoid arthritis, with TRPA1 and TRPV1 involved in the anti-inflammatory effects of N-acylethanolamines in rheumatoid arthritis synovial cells [153]. …”

Section: Impact Of Cs On Trp Channels In the Gut?mentioning

confidence: 99%

Transient Receptor Potential Channels in Intestinal Inflammation: What Is the Impact of Cigarette Smoking?

Allais

Smet²,

Verschuere³

et al. 2016

Pathobiology

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Inflammatory bowel disease (IBD) is characterized by severe gastrointestinal inflammation and results from a complex interplay between genetic and environmental factors. IBD includes two prominent subtypes: Crohn's disease (CD) and ulcerative colitis (UC). One of the main risk factors for the development of CD is cigarette smoking, while UC is rather a disease of ex-smokers. To date, many of the mechanisms underlying the immune imbalance in IBD and the involvement of cigarette smoke (CS) are incompletely understood. Transient receptor potential (TRP) proteins are non-selective cation channels that, upon activation, lead to plasma membrane depolarization and, in general, to Ca²⁺ influx. TRP channels of the ankyrin and vanilloid family, expressed by sensory neurons in the central and enteric nervous systems, have been extensively studied in the context of intestinal inflammation. Moreover, recent advances made on the role of non-neuronal expressed TRP channels shed light on the involvement of epithelial cells in inflammatory processes. This review focuses on how CS may impact TRP channel function in intestinal inflammation. Firstly, we discuss the current knowledge on neuronal TRP channels, known to be linked to IBD, in health, immune homeostasis and intestinal inflammation. Subsequently, we address how TRP channels are activated by CS and its components in other organ systems and also hypothesize on the potential implications for CS-mediated TRP channel activation in gut inflammation.

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“…These results point to a dysregulation in PEA metabolism in articular diseases and suggest that PEA supplementation may prove beneficial in these situations. In support of this hypothesis, administration of PEA or inhibition of endocannabinoid degradation ameliorates collagen‐induced arthritis in mice . Moreover, PEA administration exerts anti‐inflammatory and analgesic effects in different conditions of chronic inflammation, modulates mast cell degranulation, and reduces activation of spinal cord microglia .…”

Section: Potential New Targets For the Treatment Of Degenerative Joinmentioning

confidence: 77%

Degenerative Joint Diseases and Neuroinflammation

Fusco¹,

Skaper

Coaccioli

et al. 2017

Pain Practice

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Rheumatic and joint diseases, as exemplified by osteoarthritis and rheumatoid arthritis, are among the most widespread painful and disabling pathologies across the globe. Given the continuing rise in life expectancy, their prevalence is destined to grow. Osteoarthritis, a degenerative joint disease, is, in particular, on its way to becoming the fourth leading cause of disability worldwide by 2020, with the rising incidence of obesity in addition to age being important factors. It is estimated that 25% of osteoarthritic individuals are unable to perform daily activities. Accompanying osteoarthritis is rheumatoid arthritis, which is a chronic systemic disease that often causes pain and deformity. At least 50% of those affected are unable to remain gainfully employed within 10 years of disease onset. A growing body of evidence now points to inflammation, locally and more systemically, as a promoter of damage to joints and bones, as well as joint-related functional deficits. The pathogenesis underlying joint diseases remains unclear; however, it is currently believed that cross-talk between cartilage and subchondral bone-and loss of balance between these two structures in joint diseases-is a critical element. This view is amplified by the presence of mast cells, whose dysregulation is associated with alterations of junction structures (cartilage, bone, synovia, matrix, nerve endings, and blood vessels). In addition, persistent activation of mast cells facilitates the development of spinal neuroinflammation mediated through their interaction with microglia. Unfortunately, current treatment strategies for rheumatic and articular disease are symptomatic and do little to limit disease progression. Research now should be directed at therapeutic modalities that target osteoarticular structural elements and thereby delaying disease progression and joint replacement.

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Anti-inflammatory effects of N-acylethanolamines in rheumatoid arthritis synovial cells are mediated by TRPV1 and TRPA1 in a COX-2 dependent manner

Cited by 81 publications

References 36 publications

Joint problems arising from lack of repair mechanisms: can cannabinoids help?

Joint problems arising from lack of repair mechanisms: can cannabinoids help?

Transient Receptor Potential Channels in Intestinal Inflammation: What Is the Impact of Cigarette Smoking?

Degenerative Joint Diseases and Neuroinflammation

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