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

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


  • Morham SG
  • Langenbach R
  • Loftin CD
  • Tiano HF
  • Vouloumanos N
  • Jennette JC
  • Mahler JF
  • Kluckman KD
  • Ledford A
  • Lee CA
  • Smithies O



Publication Data

November 3, 1995

Associated Grants

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

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