Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Female homozygotes are not fertile. The protein gene product does not have cyclooxygenase activity while the peroxidase activity is normal as measured by LPS induction of macrophages derived from mutant mice. Mutant mice are more sensitive to collagen treatment resulting in reduction of platelet numbers (indicating enhanced thrombogenesis) and exhibit a higher frequency of sudden death due to thromboxane receptor agonist treatment. No prolonged bleeding time from LPS administration is observed. Prostaglandin E metabolite levels are diminished in urine. Three month old mutant mice have elevated systolic blood pressure (measured by the tail cuff method). Homozygotes exhibit undersize, pale kidneys with atrophic cortices, interstitial inflammation, hypoplastic glomeruli and glomerulosclerosis.
This mutant mouse strain may be useful in studies of thrombogenesis and hypertension.


These mutant mice have an amino acid substitution that inactivates the cyclooxygenase activity but not the peroxidase activity of the gene product. Mutant mice exhibit abnormal kidney development and function as well as elevated systolic blood pressure, which may make them useful in studies of thrombogenesis and hypertension.

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B6.129S6(FVB)-Ptgs2<tm1.1Fun>/J Frozen Embryo