Enhanced expression of cyclooxygenase-2 and prostaglandin E2 in response to endotoxin after trauma is dependent on MAPK and NF-kappaB mechanisms.

No abstract is available for this paper.

• Publication year

  2004

• Venue

  Cellular Immunology

• Publication date

  2004-11-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/J.CELLIMM.2005.03.001PMID 15890324
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Altered cyclooxygenase-2 expression and nitric oxide metabolism following major elective surgery.

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• Hemozoin Increases IFN-γ-Inducible Macrophage Nitric Oxide Generation Through Extracellular Signal-Regulated Kinase- and NF-κB-Dependent Pathways 1

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• Cyclooxygenase 2-mediated suppression of macrophage interleukin-12 production after thermal injury.

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• Oxidized phospholipids inhibit cyclooxygenase-2 in human macrophages via nuclear factor-kappaB/IkappaB- and ERK2-dependent mechanisms.

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  2001cited by this paper
• The Induction of Cyclooxygenase-2 mRNA in Macrophages Is Biphasic and Requires both CCAAT Enhancer-binding protein β (C/EBPβ) and C/EBPδ Transcription Factors*

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• Desferrioxamine, an iron chelator, upregulates cyclooxygenase-2 expression and prostaglandin production in a human macrophage cell line.

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• Hyaluronan-induced cyclooxygenase-2 expression promotes thromboxane A2 production by renal cells.

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• Fluid Shear Stress-induced Cyclooxygenase-2 Expression Is Mediated by C/EBP β, cAMP-response Element-binding Protein, and AP-1 in Osteoblastic MC3T3-E1 Cells*

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  1998cited by this paper
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  1998cited by this paper
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  1998cited by this paper
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