15-deoxy-Δ12,14-prostaglandin J2 reduces albumin-induced arthritis in temporomandibular joint of rats

Quinteiro, Mariana; Napimoga, Marcelo Henrique; Macedo, Cristina Gomes de; Freitas, Fabiana Furtado; Abdalla, Henrique Ballassini; Bonfante, Ricardo; Clemente-Napimoga, Juliana Trindade

doi:10.1016/j.ejphar.2014.07.002

Cited by 36 publications

(11 citation statements)

References 38 publications

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“…There have been several studies demonstrating a degradation product of PGD 2 , and 15d-PGJ 2 represents the anti-inflammatory effects via peroxisome proliferatoractivated receptor-g. Indeed, a previous study reported that intraperitoneal injection of 15d-PGJ 2 ameliorated adjuvant-induced arthritis accompanied with a decrease of leukocyte infiltration and pannus formation in rats (32). However, we could not detect 15d-PGJ 2 in the inflamed paws of both lines of mice.…”

Section: Discussioncontrasting

confidence: 78%

Hematopoietic prostaglandin D synthase–derived prostaglandin D₂ameliorates adjuvant‐induced joint inflammation in mice

et al. 2019

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Although prostaglandins (PGs) are known to be involved in the progression of arthritis, the role of PGD2 remains unclear. In this study, we evaluated the role of PGD2 in joint inflammation using genetically modified mice. Injection of complete Freund's adjuvant (CFA) increased the production of PGD2 and induced paw swelling and cartilage erosion in wild‐type (WT) mice. These phenomena were accompanied with an increase in the mRNA levels of TNF‐α, IL‐6, IL‐1β, and matrix‐degrading metalloproteinase‐9. Knockdown of hematopoietic PGD synthase (H‐PGDS) abolished the PGD2 production and exacerbated all of the arthritic manifestations in the inflamed paw. Immunostaining revealed that infiltrating macrophages strongly expressed H‐PGDS in the CFA‐injected paw. Morphologic studies revealed vascular hyperpermeability and angiogenesis in the inflamed WT paw. H‐PGDS deficiency was accelerated, whereas daily administration of a PGD2 receptor D prostanoid (DP) agonist attenuated the CFA‐induced hyperpermeability and angiogenesis. We further confirmed that DP deficiency exacerbated, whereas the administration of the DP agonist improved, the CFA‐induced arthritic manifestations. The findings demonstrate that H‐PGDS–derived PGD2 ameliorates joint inflammation by attenuating vascular permeability and subsequent angiogenesis and indicates the therapeutic potential of a DP agonist for arthritis.—Tsubosaka, Y., Maehara, T., Imai, D., Nakamura, T., Kobayashi, K., Nagata, N., Fujii, W., Murata, T. Hematopoietic prostaglandin D synthase–derived prostaglandin D2 ameliorates adjuvant‐induced joint inflammation in mice. FASEB J. 33, 6829–6837 (2019). http://www.fasebj.org

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Section: Discussioncontrasting

confidence: 78%

Hematopoietic prostaglandin D synthase–derived prostaglandin D₂ameliorates adjuvant‐induced joint inflammation in mice

et al. 2019

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“…Granulocyte colony-stimulating factor, macrophage colony-stimulating factor, and granulocyte–macrophage colony-stimulating factor (GM-CSF) promote the maturation of the above innate effector cells, trafficking to the synovium, and their efflux from the bone marrow [ 49 , 50 ]. Importantly, macrophages act as central effectors of synovitis and are effective biologic agents that could reduce macrophage infiltration consistently in the synovium [ 51 , 52 ]. Macrophages act via release of cytokines, for instance, TNF-α and IL-1, -6, -12, -15, -18, and -23, with TNF-α and IL-6 being the most predominant mediators, eventually resulting in the breakdown of extracellular matrix of bone and cartilage [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

Serum Levels of IL-6 and TNF-α May Correlate with Activity and Severity of Rheumatoid Arthritis

Wei¹,

Sun²,

Zong³

et al. 2015

Med Sci Monit

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BackgroundWe aimed to investigate the association of rheumatoid arthritis (RA) with interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) through a meta-analysis.Material/MethodsThe case-control studies that investigated the association between RA and serum levels of IL-6 and TNF-α were retrieved strictly according to the inclusion and exclusion criteria. The statistical analysis was performed using STATA statistical software (Version 12.0, Stata Corporation, College Station, TX, USA).ResultsFourteen studies were enrolled in our meta-analysis, with a total of 890 patients with RA and 441 healthy people as the controls. The results of this meta-analysis revealed that the serum IL-6 and TNF-α levels of RA patients were significantly higher than in the controls, and this difference was statistically significant (IL-6: SMD=2.40, 95% CI=1.57~3.24, P<0.001; TNF-α: SMD=1.93, 95% CI=1.23~2.64, P<0.001). According to ethnic subgroup analysis, the serum IL-6 and TNF-α levels of RA patients were also significantly higher compared with the controls in Asians and Caucasians (IL-6: Asians: SMD=3.64, 95% CI=2.16~5.12, P<0.001; Caucasians: SMD=0.75, 95% CI=0.47~1.02, P<0.001; TNF-α: Asians: SMD=2.74, 95%CI=1.58~3.91, P<0.001; Caucasians: SMD=0.81, 95% CI=0.50~1.11, P<0.001).ConclusionsIL-6 and TNF-α may play crucial roles in the activity and severity of RA.

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“…15d-PGJ 2 is an important prostaglandin in the resolution of inflammation [39]. This is also true for chondrocytes from OA patients [40-42]. Therefore, the switch in prostaglandin synthesis seems to be a major factor in stopping inflammation and initiating healing in OA cartilage.…”

Section: Contribution Of Anti-inflammatory Prostaglandins In Oamentioning

confidence: 99%

Inflammatory Pathways in Knee Osteoarthritis: Potential Targets for Treatment

Bar‐Or¹,

Rael²,

Thomas³

et al. 2015

CRR

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Osteoarthritis (OA) of the knee is a wide-spread, debilitating disease that is prominent in Western countries. It is associated with old age, obesity, and mechanical stress on the knee joint. By examining the recent literature on the effect of the anti-inflammatory prostaglandins 15d-PGJ2 and Δ12-PGJ2, we propose that new therapeutic agents for this disease could facilitate the transition from the COX-2-dependent pro-inflammatory synthesis of the prostaglandin PGE2 (catalyzed by mPGES-1), to the equally COX-2-dependent synthesis of the aforementioned anti-inflammatory prostaglandins. This transition could be instrumental in halting the breakdown of cartilage via matrix metalloproteinases (MMPs) and aggrecanases, as well as promoting the matrix regeneration and synthesis of cartilage by chondrocytes. Another desirable property of new OA therapeutics could involve the recruitment of mesenchymal stem cells to the damaged cartilage and bone, possibly resulting in the generation of chondrocytes, synoviocytes, and, in the case of bone, osteoblasts. Moreover, we propose that research promoting this transition from pro-inflammatory to anti-inflammatory prostaglandins could aid in the identification of new OA therapeutics.

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15-deoxy-Δ12,14-prostaglandin J2 reduces albumin-induced arthritis in temporomandibular joint of rats

Cited by 36 publications

References 38 publications

Hematopoietic prostaglandin D synthase–derived prostaglandin D₂ameliorates adjuvant‐induced joint inflammation in mice

Hematopoietic prostaglandin D synthase–derived prostaglandin D₂ameliorates adjuvant‐induced joint inflammation in mice

Serum Levels of IL-6 and TNF-α May Correlate with Activity and Severity of Rheumatoid Arthritis

Inflammatory Pathways in Knee Osteoarthritis: Potential Targets for Treatment

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15-deoxy-Δ12,14-prostaglandin J2 reduces albumin-induced arthritis in temporomandibular joint of rats

Cited by 36 publications

References 38 publications

Hematopoietic prostaglandin D synthase–derived prostaglandin D2ameliorates adjuvant‐induced joint inflammation in mice

Hematopoietic prostaglandin D synthase–derived prostaglandin D2ameliorates adjuvant‐induced joint inflammation in mice

Serum Levels of IL-6 and TNF-α May Correlate with Activity and Severity of Rheumatoid Arthritis

Inflammatory Pathways in Knee Osteoarthritis: Potential Targets for Treatment

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Product

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Hematopoietic prostaglandin D synthase–derived prostaglandin D₂ameliorates adjuvant‐induced joint inflammation in mice

Hematopoietic prostaglandin D synthase–derived prostaglandin D₂ameliorates adjuvant‐induced joint inflammation in mice