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Prostaglandin synthase 1 gene disruption in mice reduces arachidonic acid-induced inflammation and indomethacin-induced gastric ulceration.

Cyclooxygenases 1 and 2 (COX-1 and COX-2) are key enzymes in prostaglandin biosynthesis and the target enzymes for the widely used nonsteroidal anti-inflammatory drugs. To study the physiological roles of the individual isoforms, we have disrupted the mouse Ptgs1 gene encoding COX-1. Homozygous Ptgs1 mutant mice survive well, have no gastric pathology, and show less indomethacin-induced gastric ulceration than wild-type mice, even though their gastric prostaglandin E2 levels are about 1% of wild type. The homozygous mutant mice have reduced platelet aggregation and a decreased inflammatory response to arachidonic acid, but not to tetradecanoyl phorbol acetate. Ptgs1 homozygous mutant females mated to homozygous mutant males produce few live offspring. COX-1-deficient mice provide a useful model to distinguish the physiological roles of COX-1 and COX-2.

Pubmed ID: 8521478


  • Langenbach R
  • Morham SG
  • Tiano HF
  • Loftin CD
  • Ghanayem BI
  • Chulada PC
  • Mahler JF
  • Lee CA
  • Goulding EH
  • Kluckman KD
  • Kim HS
  • Smithies O



Publication Data

November 3, 1995

Associated Grants

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

Mesh Terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal
  • Arachidonic Acid
  • Blotting, Northern
  • Blotting, Western
  • Cloning, Molecular
  • Dinoprostone
  • Female
  • Gastritis
  • Genetic Vectors
  • Homozygote
  • Indomethacin
  • Macrophages, Peritoneal
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mutation
  • Otitis Externa
  • Phenotype
  • Plasmids
  • Platelet Aggregation
  • Prostaglandin-Endoperoxide Synthases
  • Stomach Ulcer