INT28420
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
PGD2 is further dehydrated to produce PGJ2, delta12-PGJ2, and 15-deoxy-delta(12,14)-PGJ2, the last being a ligand for the nuclear receptor PPARgamma. | |||||||||||||||
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It can be assumed, that PGD2 biosynthesis under control conditions is mediated via COX-1 and that during inflammation, increased PGD2 is dependent on COX-2. | |||||||||||||||
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An initial rapid burst of PGD2 synthesis, complete within 30 min, is followed by a slower subsequent production of PGD2 that reaches a maximum 4 to 8 h after activation in MMC-34 cells. | |||||||||||||||
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These data demonstrate that mast cell activation results 1) in the induction of PGS-2 gene expression, and 2) in both PGS-1-dependent PGD2 synthesis and PGD2 synthesis that is dependent on the activation-induced synthesis and activity of PGS-2. | |||||||||||||||
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In an endotoxin-based mouse model of inflammation, administration of aspirin or indomethacin nearly abolished both PGE2 and PGD2 synthesis, whereas PGD2 levels rose during the natural resolution of inflammation in untreated animals [33]. | |||||||||||||||
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raises PGE2, but decreases PGD2, synthesis by zymosan-stimulated murine macrophages [37]. | |||||||||||||||
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In an endotoxin-based mouse model of inflammation, administration of aspirin or indomethacin nearly abolished both PGE2 and PGD2 synthesis, whereas PGD2 levels rose during the natural resolution of inflammation in untreated animals [33]. | |||||||||||||||
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Dexamethasone induces lipocalin-type prostaglandin D synthase gene expression in mouse neuronal cells. | |||||||||||||||
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Prostaglandin D2 (PGD2), the predominant prostanoid produced by activated mast cells, is implicated in a variety of allergic diseases. | |||||||||||||||
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Prostaglandin D2 (PGD2), the predominant prostanoid produced by activated mast cells, is implicated in a variety of allergic diseases. | |||||||||||||||
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We found the PGD2 receptors DP1 and chemoattractant receptor homologous molecule expressed on T helper type 2 cells (CRTH2) localized in neurons of the dorsal, and motoneurons in the ventral horn. | |||||||||||||||
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Effect of endotoxin treatment on the expression and localization of spinal cyclooxygenase, prostaglandin synthases, and PGD2 receptors. | |||||||||||||||
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An initial rapid burst of PGD2 synthesis, complete within 30 min, is followed by a slower subsequent production of PGD2 that reaches a maximum 4 to 8 h after activation in MMC-34 cells. | |||||||||||||||
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In contrast, the later phase of PGD2 production is blocked by dexamethasone, cycloheximide, or NS-398, a PGS-2-specific nonsteroidal anti-inflammatory drug that inhibits PGS-2 enzyme activity but not PGS-1 activity. | |||||||||||||||
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Dexamethasone inhibited PGD2 synthesis in zymosan-stimulated murine macrophages [37]. | |||||||||||||||
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Prednisone did not alter PGD2 synthesis during the cutaneous late-phase allergic response in humans [40]. | |||||||||||||||
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Exudate IL-6, PGE2 and PGD2 levels were determined by commercially available immunoassays (eBioscience, San Diego, CA, USA (IL-6) and Cayman Chemical, Ann Arbor, MI, USA (PGE2 and PGD2)).
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How do commonly used anti-inflammatory agents, such as NSAIDs and corticosteroids, affect PGD2 levels? | |||||||||||||||
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In contrast, in acute peritoneal inflammation, knockout of PGD2 synthase increased inflammatory cytokine production and retarded the rate of inflammatory resolution by a mechanism that operated through the DP-1 receptor [24]. | |||||||||||||||
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The provision of exogenous PGD2 but not PGD3 (which could be derived from EPA), fully restored the ability of neutrophils to cross the endothelial cell monolayer (Figure 7A). | |||||||||||||||
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