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Prostaglandin synthase 2 gene disruption causes severe renal pathology in the mouse.

Cell | Nov 3, 1995

http://www.ncbi.nlm.nih.gov/pubmed/8521477

The prostaglandin endoperoxide H synthase isoform 2, cyclooxygenase 2 (COX-2), is induced at high levels in migratory and other responding cells by pro-inflammatory stimuli. COX-2 is generally considered to be a mediator of inflammation. Its isoform, COX-1, is constitutively expressed in most tissues and is thought to mediate "housekeeping" functions. These two enzymes are therapeutic targets of the widely used nonsteroidal anti-inflammatory drugs (NSAIDs). To investigate further the different physiologic roles of these isoforms, we have used homologous recombination to disrupt the mouse gene encoding COX-2 (Ptgs2). Mice lacking COX-2 have normal inflammatory responses to treatments with tetradecanoyl phorbol acetate or with arachidonic acid. However, they develop severe nephropathy and are susceptible to peritonitis.

Pubmed ID: 8521477 RIS Download

Mesh terms: Animals | Arachidonic Acid | Bacteriophage lambda | Base Sequence | Dinoprostone | Female | Genetic Vectors | Genotype | Homozygote | Kidney | Lipopolysaccharides | Macrophages, Peritoneal | Male | Mice | Mice, Mutant Strains | Molecular Sequence Data | Mortality | Otitis Externa | Peritoneum | Prostaglandin-Endoperoxide Synthases | Tetradecanoylphorbol Acetate

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Associated grants

  • Agency: NIGMS NIH HHS, Id: GM20069
  • Agency: NHLBI NIH HHS, Id: HL49227

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