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J. Biol. Chem., Vol. 279, Issue 11, 10649-10658, March 12, 2004
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Rescue of Female Infertility from the Loss of Cyclooxygenase-2 by Compensatory Up-regulation of Cyclooxygenase-1 Is a Function of Genetic Makeup*
From the Departments of aPediatrics, eClinical Pharmacology, gCancer Biology, hCell and Developmental Biology, and iPharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232
Cyclooxygenase-2 (COX-2), an inducible rate-limiting enzyme in prostaglandin biosynthesis, is implicated in various physiological and pathological processes including female fertility, renal function, angiogenesis, inflammation, and tumorigenesis. We showed previously that targeted deletion of Ptgs2 encoding COX-2, but not Ptgs1 encoding COX-1, in C57BL/6J/129 mice produces complete female infertility resulting from multiple reproductive failures spanning ovulation, fertilization, and implantation. Here we show that Ptgs2 null mice on a CD1 background have dramatically improved female fertility including ovulation, fertilization, and implantation, giving rise to live births. We provide evidence that this improved fertility in CD1 Ptgs2 null mice is the result of a compensatory up-regulation of Ptgs1 which does not occur in C57BL/6J/129 mice missing Ptgs2. These results clearly demonstrate for the first time that COX-1 can replace specific functions of COX-2 in vivo in the context of genetic disparity. In light of this finding, the therapeutic use and efficacy of COX-2-specific inhibitors among human populations without regard for genetic and ethnic diversities should be revisited.
Received for publication, November 7, 2003 , and in revised form, December 22, 2003.
* This work was supported in part by National Institutes of Health Grants HD12304, HD33994, and DA06668 (to S. K. Dey), DK48831, CA77839, and GM15431 (to J. D. M.), and HD37830 and ES07814 (to S. K. Das). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
b Lalor Foundation postdoctoral fellow.
c Present address: Dept. of Oral Biology, University of California, San Francisco, CA 94143.
d Present address: Dept. of Physiology, University of Kansas Medical Center, Kansas City, KS 66103.
f Recipient of a Burroughs Wellcome Fund clinical scientist award in translational research.
j To whom correspondence should be addressed: Dept. of Pediatrics, Division of Reproductive and Developmental Biology, Vanderbilt University Medical Center, MCN-D4100, Nashville, TN 37232. Tel.: 615-322-8642; Fax: 615-322-4704; E-mail: sk.dey{at}vanderbilt.edu.
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