A systematic review on the role of eicosanoid pathways in rheumatoid arthritis

Hoxha, Malvina

doi:10.1016/j.advms.2017.06.004

Cited by 69 publications

(47 citation statements)

References 79 publications

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“…The results obtained in our study have shown that levels of PUFAs decrease in both forms of psoriasis, but more in the case of PsA, which had more pronounced onset of oxidative stress, as discussed already. Similar systemic alterations of the PUFA metabolism were also observed in other inflammatory diseases such as rheumatoid arthritis (RA) [60,61]. The ROS-dependent peroxidation of PUFAs generates a broad range of products including compounds produced during oxidative cyclisation as well as fragmentation [6,62].…”

Section: Discussionmentioning

confidence: 63%

Pathophysiological Alterations of Redox Signaling and Endocannabinoid System in Granulocytes and Plasma of Psoriatic Patients

Ambrożewic¹,

Wójcik²,

Wroński³

et al. 2018

Preprint

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Inflammatory granulocytes are characterized by oxidative burst, which may promote oxidative stress and lipid modification both in affected tissues and on systemic level. On the other hand, redox signaling involving lipid peroxidation products acting as second messengers of free radicals play important, not yet fully understood, roles in pathophysiology of inflammation and various stress-associated disorders. Therefore, the aim of this study was to evaluate the onset of oxidative stress and alterations of enzyme-dependent lipid metabolism resulting from redox imbalance in granulocytes and plasma obtained from patients with psoriasis vulgaris or psoriatic arthritis, in comparison to the healthy subjects.The results obtained revealed enhanced activity of pro-oxidant enzymes NADPH and xanthine oxidases in granulocytes, with a decrease of enzymatic and non-enzymatic antioxidants in plasma of psoriatic patients. The Nrf2 and its regulators were increased in both forms of psoriasis, while HO-1 levels were increased only in psoriasis vulgaris. Redox imbalance was associated with decreased levels of phospholipids and of free PUFAs, but with enhanced activity of enzymes involved in lipid metabolism (PLA2, PAF-AH COX1/2) and increased lipid peroxidation products 4-hydroxynonenal (4-HNE), isoprostanes and neuroprostanes. Increased endocannabinoids and GPR55 were observed in both forms of the disease, while expression of CB1 was increased only in pateints with psoriatic arthritis, opposite to CB2, which was increased only in psoriasis vulgaris. Protein modifications by ROS and lipid peroxidation product 4-HNE promoted apoptosis of granulocytes by increased caspases in both forms of psoriasis.This study indicates that excessive activation of granulocytes, causing oxidative stress and lipid modifications, is an important pathophysiology of psoriasis. Consequently, lower Nrf2 activity and CB2 expression may promote progression of psoriasis into advanced, arthritic form of the disease.

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Section: Discussionmentioning

confidence: 63%

Pathophysiological Alterations of Redox Signaling and Endocannabinoid System in Granulocytes and Plasma of Psoriatic Patients

Ambrożewic¹,

Wójcik²,

Wroński³

et al. 2018

Preprint

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“…Other SAGs that directly and indirectly contribute to the sustained and exacerbated NF-B signaling included the TNFAIP3, which encodes the deubiquitinating enzyme A20, that plays a role in the NF-B noncanonical activation (22). The C-C motif and multiple C-X-C motif chemokine ligands (23) and prostaglandin synthesis pathway components were other additional pro-inflammatory pathways that show sustained activation in the RA FLS (24). Together these data have uncovered that FLS attain a robust long-term inflammatory memory in response to chronic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Chronic exposure to TNF reprograms cell signaling pathways in fibroblast-like synoviocytes by establishing long-term inflammatory memory

Gangishetti

Ramírez-Pérez

Jones

et al. 2020

Preprint

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Fibroblast-like synoviocytes (FLS) play a critical role in the pathogenesis of rheumatoid arthritis (RA). Chronic inflammation induces transcriptomic and epigenetic modifications that imparts a persistent catabolic phenotype to the FLS, despite their dissociation from the inflammatory environment. We analyzed high throughput gene expression and chromatin accessibility data from human and mouse FLS from our and other studies available on public repositories, with the goal of identifying the persistently reprogrammed signaling pathways driven by chronic inflammation. We found that the gene expression changes induced by short-term tumor necrosis factor-alpha (TNF) treatment were largely sustained in the FLS exposed to chronic inflammation. These changes that included both activation and repression of gene expression, were accompanied by the remodeling of chromatin accessibility. The sustained activated genes (SAGs) included established proinflammatory signaling components known to act at multiple levels of NF-kappaB, STAT and AP-1 signaling cascades. Interestingly, the sustained repressed genes (SRGs) included critical mediators and targets of the BMP signaling pathway. We thus identified sustained repression of BMP signaling as a unique constituent of the long-term inflammatory memory induced by chronic inflammation. We postulate that simultaneous targeting of these activated and repressed signaling pathways may be necessary to combat RA persistence. on a Hi-Seq 2500 System (University of Georgia Genomics Core) to generate data in FastQ file format. In order to study chromatin accessibility changes due to chronic inflammation, we downloaded FastQ files from a DNase I hypersensitivity sequencing (DNase-seq) experiment of wild-type FLS and inflamed FLS from inflammatory arthritis mouse model (Table S1). FastQ files from the ATAC-seq and DNase-seq experiments were analyzed using the Strand NGS sequence analysis pipeline first by aligning the sequences to the mouse genome, mm10 build, followed by removal of duplicate reads.Peak calling and gene annotation were performed by MACS2 algorithm using a padding distance of 5 kb from the transcription start sites of genes. Pathway analysis. Ingenuity Pathway Analysis tool was used to predict the canonical regulatory pathways and diseases and functions associated with the SAGs and SRGs (38). Functional protein-protein analysis was performed using STRING protein-protein interaction plugin on Cytoscape, an open source software platform for visualizing complex networks pathway analysis tool (39, 40). Open-source tool, ChEA3 that uses ChIP-seq experiments from the ENCODE database was used to predict transcription factors associations with SAG and SRGs (17).

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“…Lipid derivatives from arachidonic acid are increased in RA synovium and play an inflammatory role; drug targeting enzymes of arachidonic acid metabolismcyclooxygenase inhibitors-are useful for controlling the pain caused in arthritis [49]. Proinflammatory cytokines, IL-1β, IL-6, IL-17, and TNF-α, are elevated in https://doi.org/10.3904/kjim.2019.271…”

Section: Lipid Derivatives and Proinflammatory Cytokine From MC In Ramentioning

confidence: 99%

“…The metabolites of arachidonic acid depend on the enzymes. Lipoxygenase mediates the production of leukotrienes, and cyclooxygenases mediates prostaglandins and thromboxane production [49]. Leukotriene B4 (LTB4), PGE2, and prostaglandin I2 (PGI2) induce an inflammatory response in RA pathogenesis [49].…”

Section: Lipid Derivatives and Proinflammatory Cytokine From MC In Ramentioning

confidence: 99%

Roles of mast cells in rheumatoid arthritis

Min

Kim

Lee

et al. 2020

Korean J Intern Med

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Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory arthritis, and the complex interaction and activation of innate and adaptive immune cells are involved in RA pathogenesis. Mast cells (MCs) are one of the tissue-resident innate immune cells, and they contribute to RA pathogenesis. In the present review, the evidence of the pathologic role of MC in RA is discussed based on human and animal data. In addition, the potential role of MC in RA pathogenesis and the research area that should be focused on in the future are suggested.

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A systematic review on the role of eicosanoid pathways in rheumatoid arthritis

Cited by 69 publications

References 79 publications

Pathophysiological Alterations of Redox Signaling and Endocannabinoid System in Granulocytes and Plasma of Psoriatic Patients

Pathophysiological Alterations of Redox Signaling and Endocannabinoid System in Granulocytes and Plasma of Psoriatic Patients

Chronic exposure to TNF reprograms cell signaling pathways in fibroblast-like synoviocytes by establishing long-term inflammatory memory

Roles of mast cells in rheumatoid arthritis

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