Mice homozygous for the Ptgs2tm1Jed targeted mutation exhibit significant preweaning loss of homozygotes (original publication reports 30-40%). Homozygous mutant mice show polydipsia and polyuria due to a defect in renal development. Cardiac fibrosis is evident in approximately 50% of the mice. PTGS2 deficient mice do not show altered inflammatory responses to in several tests of paw and ear edema; however, cytoxicity of hepatic cells induced by endotoxin was strikingly mitigated in these homozygotes. Female homozygotes are infertile with defects in ovulation, fertilization, implantation, and decidualization.

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These Ptgs2 knock-out mice exhibit reduced viability with cardiac fibrosis and renal alterations characteristic of renal dysplasia. They are suitable for use in applications related to the study of mediators of inflammation.

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