Sequential induction of pro- and anti-inflammatory prostaglandins and peroxisome proliferators-activated receptor-gamma during normal wound healing: A time course study

Kapoor, Mohit; Kojima, Fumio; Yang, Lihua; Crofford, Leslie J.

doi:10.1016/j.plefa.2006.11.006

Cited by 60 publications

(56 citation statements)

References 40 publications

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“…75 However, no up-regulation of mPGES-2 expression was observed under inflammatory conditions in murine mPGES-1 null fibroblasts or macrophages. 76,77 Moreover, we have previously reported that neither small interfering RNA (siRNA) knockdown nor chemical mPGES-1 inhibition affects the expression of cPGES or mPGES-2 in human gingival fibroblasts. 31 Our experiments with mPGES-1 null gingival fibroblasts clearly demonstrated that mPGES-1 is important for basal production of PGE 2 and critical for PGE 2 production under inflammatory condition.…”

Section: Discussionmentioning

confidence: 99%

Expression of Prostaglandin E Synthases in Periodontitis

Båge

Kats

Lopez

et al. 2011

The American Journal of Pathology

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The inflammatory mediator prostaglandin E 2 (PGE 2 ) is implicated in the pathogenesis of chronic inflammatory diseases including periodontitis; it is synthesized by cyclooxygenases (COX) and the prostaglandin E synthases mPGES-1, mPGES-2, and cPGES. The distribution of PGES in gingival tissue of patients with periodontitis and the contribution of these enzymes to inflammationinduced PGE 2 synthesis in different cell types was investigated. In gingival biopsies, positive staining for PGES was observed in fibroblasts and endothelial, smooth muscle, epithelial, and immune cells. To further explore the contribution of PGES to inflammation-induced PGE 2 production, in vitro cell culture experiments were performed using fibroblasts and endothelial, smooth muscle, and mast cells. All cell types expressed PGES and COX-2, resulting in basal levels of PGE 2 synthesis. In response to tumor necrosis factor (TNF-␣), IL-1␤, and cocultured lymphocytes, however, mPGES-1 and COX-2 protein expression increased in fibroblasts and smooth muscle cells, accompanied by increased PGE 2 , whereas mPGES-2 and cPGES were unaffected. In endothelial cells, TNF-␣ increased PGE 2 production only via COX-2 expression, whereas in mast cells the cytokines did not affect PGE 2 enzyme expression or PGE 2 production. Furthermore, PGE 2 production was diminished in gingival fibroblasts derived from mPGES-1 knockout mice, compared with wild-type fibroblasts. These results suggest that fibroblasts and smooth muscle cells are important sources of mPGES-1, which may contribute to increased PGE 2 production in the inflammatory condition periodontitis.

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Section: Discussionmentioning

confidence: 99%

Expression of Prostaglandin E Synthases in Periodontitis

Båge

Kats

Lopez

et al. 2011

The American Journal of Pathology

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“…PGD 2 is considered to be an anti-inflammatory mediator. 34,35 The dehydration endproduct of PGD 2 is PGJ 2 , which represses several proinflammatory genes including tumor necrosis factor (TNF)-␣, interleukin-1␤, and inducible nitric oxide synthase. 36,37 Even though the replacement of arachidonic acids with EPA reduces the generation of arachidonic acid metabolites in general; an increased PGI 2 after fish oil supplementation has been reported.…”

Section: Cx3cr1mentioning

confidence: 99%

A High Omega-3 Fatty Acid Diet Reduces Retinal Lesions in a Murine Model of Macular Degeneration

Tuo

Ross

Herzlich

et al. 2009

The American Journal of Pathology

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Age-related macular degeneration (AMD) is one of the leading cause of blindness among the elderly; however, current therapy options are limited. Epidemiological studies have shown that a diet that is high in -3 polyunsaturated (n-3) fatty acids can slow disease progression in patients with advanced AMD. In this study, we evaluated the effect of such a diet on the retinas of Ccl2 ؊/؊ /Cx3cr1 ؊/؊ mice, a model that develops AMD-like retinal lesions that include focal deep retinal lesions, abnormal retinal pigment epithelium, photoreceptor degeneration, and A2E accumulation. Ccl2 ؊/؊ /Cx3cr1 ؊/؊ mice that ingested a high n-3 fatty acid diet showed a slower progression of retinal lesions compared with the low n-3 fatty acids group. Some mice that were given high levels of n-3 fatty acids had lesion reversion. We found a shunted arachidonic acid metabolism that resulted in decreased pro-inflammatory derivatives (prostaglandin E 2 and leukotriene B 4 ) and an increased antiinflammatory derivative (prostaglandin D 2 ). We also measured lower ocular TNF-␣ and IL-6 transcript levels in the mice fed a diet of high n-3 fatty acids. Our findings in these mice are in line with human studies of AMD risk reduction by long-chain n-3 fatty acids. This murine model provides a useful tool to evaluate therapies that might delay the development of AMD.

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“…PPARc1 is widely expressed in many tissues, including inflammatory and immune cells, whereas PPARc2 is found mainly in adipose tissues. PPARc plays important roles in the regulation of glucid and lipid metabolism, and has been implicated in several pathological conditions including diabetes [10], cardiovascular diseases [11], carcinogenesis [12], and inflammation [13][14][15]. Emerging evidence suggests that PPARc plays an important role in the pathogenesis of arthritis, OA, and RA, and possibly other chronic inflammatory diseases.…”

Section: Pparcmentioning

confidence: 99%

Peroxisome proliferator-activated receptor gamma in osteoarthritis

Fahmi¹,

Martel‐Pelletier²,

Pelletier³

et al. 2010

Mod Rheumatol

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Osteoarthritis (OA) is among the most prevalent chronic human health disorders and the most common form of arthritis. It is a leading cause of disability in developed countries. This disease is characterized by cartilage deterioration, synovitis, and remodeling of the subchondral bone. There is not yet a satisfactory treatment to stop or arrest this disease process. Although several candidates for therapeutic approaches have been put forward, recent studies suggest that activation of the transcription factor peroxisome proliferator-activated receptor gamma (PPARγ) is an interesting target for this disease. PPARγ is a ligand-activated transcription factor and member of the nuclear receptor superfamily. Agonists of PPARγ inhibit inflammation and reduce synthesis of cartilage degradation products both in vitro and in vivo, and reduce the development/progression of cartilage lesions in OA animal models. This review will highlight the recent experimental studies on the presence of PPARγ in articular tissues and its effect on inflammatory and catabolic responses in chondrocytes and synovial fibroblasts, as well as the protective effects of PPARγ ligands in arthritis experimental models. Finally, the role of PPARγ polymorphism in the pathogenesis of OA and related musculoskeletal diseases will also be discussed.

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Sequential induction of pro- and anti-inflammatory prostaglandins and peroxisome proliferators-activated receptor-gamma during normal wound healing: A time course study

Cited by 60 publications

References 40 publications

Expression of Prostaglandin E Synthases in Periodontitis

Expression of Prostaglandin E Synthases in Periodontitis

A High Omega-3 Fatty Acid Diet Reduces Retinal Lesions in a Murine Model of Macular Degeneration

Peroxisome proliferator-activated receptor gamma in osteoarthritis

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