Differential regulation of monocytic expression of leukotriene and lipoxin receptors

Petri, Marcelo H.; Thul, Silke; Ovchinnikova, Olga; Bäck, Magnus

doi:10.1016/j.prostaglandins.2015.07.005

Cited by 11 publications

(6 citation statements)

References 33 publications

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“…Atherosclerotic lesions derived from ATL-treated ApoE mice exhibit a decreased macrophage content and less inflammation ( Petri et al, 2017 ), consistent with the lipoxin-induced reduction of proi-nflammatory cytokines observed in monocytic cells in vitro ( Petri et al, 2015c ). Furthermore, less apoptotic cells are observed in atherosclerotic lesions after ATL treatment ( Petri et al, 2017 ).…”

Section: Alx/fpr2supporting

confidence: 61%

Lipoxin and Resolvin Receptors Transducing the Resolution of Inflammation in Cardiovascular Disease

2018

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A non-resolving inflammation results in a chronic inflammatory response, characteristic of atherosclerosis, abdominal aortic aneurysms and several other cardiovascular diseases. Restoring the levels of specialized proresolving mediators to drive the chronic cardiovascular inflammation toward resolution is emerging as a novel therapeutic principle. The lipid mediators lipoxins and resolvins exert their proresolving actions through specific G-protein coupled receptors (GPCR). So far, four GPCR have been identified as the receptors for lipoxin A4 and the D- and E-series of resolvins, namely ALX/FPR2, DRV1/GPR32, DRV2/GPR18, and ERV1/ChemR23. At the same time, other pro-inflammatory ligands also activate some of these receptors. Recent studies of genetic targeting of these receptors in atherosclerotic mouse strains have revealed a major role for proresolving receptors in atherosclerosis. The present review addresses the complex pharmacology of these four proresolving GPCRs with focus on their therapeutic implications and opportunities for inducing the resolution of inflammation in cardiovascular disease.

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Section: Alx/fpr2supporting

confidence: 61%

Lipoxin and Resolvin Receptors Transducing the Resolution of Inflammation in Cardiovascular Disease

2018

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“…Also, pre-treatment with Boc-2 blocked the inhibitory effect of supernatants obtained on differentiated macrophages from human THP-1 cells on tube formation by human HUVEC cells. It is important to note that THP-1 cells express FPRs 56,57 . Therefore, our data demonstrate, for the first time, that FPRs are essential for the immunomodulatory actions of CTX also in human cells.…”

Section: Discussionmentioning

confidence: 99%

Crotoxin promotes macrophage reprogramming towards an antiangiogenic phenotype

Pimenta

Almeida

Bretones

et al. 2019

Sci Rep

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Crotoxin (CTX) is the primary toxin of South American rattlesnake Crotalus durissus terrificus venom. CTX reduces tumour mass, and tumour cell proliferation and these effects seem to involve the formation of new vessels. Angiogenesis has a key role in tumour growth and progression and is regulated by macrophage secretory activity. Herein, the effect of CTX on macrophage secretory activity associated with angiogenesis was investigated in vitro. Thymic endothelial cells (EC) were incubated in the presence of macrophages treated with CTX (12.5 nM) or supernatants of CTX-treated macrophages and endothelial cell proliferation, migration and adhesion activities, and the capillary-like tube formation in the matrigel-3D matrix was measured. Angiogenic mediators (MMP-2, VEGF and TNF-α) were measured in the cell culture medium. Macrophages pre-treated with CTX and supernatant of CTX-treated macrophages inhibited EC proliferation, adhesion to its natural ligands, and migration (as evaluated in a wound-healing model and Time Lapse assay) activities. Decreased capillary-like tube formation and MMP-2, VEGF and TNF-α levels in the supernatant of macrophages treated with CTX was also described. CTX promotes macrophage reprogramming towards an antiangiogenic phenotype.

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“…This raises the possibility that the affects observed with Arthrocen were not mediated through eicosanoids. However, prior studies have demonstrated that monocytes perhaps utilize arachidonic acid derived from other cell types for the synthesis of eicosanoids ( Goldyne & Stobo, 1982 ; Petri, Thul, Ovchinnikova, & Bäck, 2015 ). To assess for the potential of our cells to make prostaglandins and leukotrienes (products downstream of arachidonic acid in eicosanoid biosynthesis) we assessed our RNA-Sequencing data for the transcripts involved in these pathways.…”

Section: Discussionmentioning

confidence: 99%

In Vitro Effects of Arthrocen, an Avocado/Soy Unsaponifiables Agent, on Inflammation and Global Gene Expression in Human Monocytes

Taylor¹,

Goudarzi²,

Yazdi³

et al. 2017

IJC

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Osteoarthritis (OA) is the most common form of arthritis. Symptomatically characterized by stiffness and pain, OA is a chronic degenerative disease of joints. Of note, there is growing interest in the potential use of plant-based compounds for symptomatic treatment of OA. Arthrocen is a plant-derived agent consisting of a one to two ratio of avocado and soy unsaponifiable extracts. In order to decipher the potential mechanisms of Arthrocen’s action at the molecular level, we employed an in vitro assay using cultured human THP-1 cells (a model cell line for monocytes) to study its effects. By pairing protein arrays enriched for inflammatory markers, transcriptomic pathway analysis using RNA-Sequencing, and eicosanoid specific lipidomics, we have begun to unravel its potential mechanism of action. Specifically, we found that Arthrocen can attenuate the inflammatory response at the transcript level while inducing significant changes in numerous cytokines. Furthermore, we discovered that while Arthrocen alone did not increase IL-8 or MCP-1 levels, its presence had a synergistic effect on the observed increase in response to LPS stimulation. Additionally, this synergistic effect of Arthrocen on LPS stimulation of IL-8 and MCP-1 protein levels was also observed at the mRNA level and suggests a regulatory mechanism at the transcriptional level. Interestingly, Arthrocen induced no changes in any of the eicosanoids studied. This multi-omics approach implies that Arthrocen functions at the level of gene transcription to dampen inflammation mediated by monocytes in OA.

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Differential regulation of monocytic expression of leukotriene and lipoxin receptors

Cited by 11 publications

References 33 publications

Lipoxin and Resolvin Receptors Transducing the Resolution of Inflammation in Cardiovascular Disease

Lipoxin and Resolvin Receptors Transducing the Resolution of Inflammation in Cardiovascular Disease

Crotoxin promotes macrophage reprogramming towards an antiangiogenic phenotype

In Vitro Effects of Arthrocen, an Avocado/Soy Unsaponifiables Agent, on Inflammation and Global Gene Expression in Human Monocytes

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