Genetic Control of Hormone-Induced Ovulation Rate in Mice1

Spearow, Jimmy L.; Barkley, M. S.

doi:10.1095/biolreprod61.4.851

Cited by 53 publications

(34 citation statements)

References 28 publications

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“…Collectively, our results of genetic and expression studies demonstrate for the first time the relative contribution of granulosa and cumulus cell COX isoforms in ovulation and fertilization. Although the mechanism of differential COX isoform regulation in C57BL/6J/129 and CD1 ovaries is not known, there is now evidence that multiple quantitative trait loci control strain differences in the ovulation rate (29). It is conceivable that the reproductive traits are different between C57BL/6J/129 and CD1 mice.…”

Section: Discussionmentioning

confidence: 99%

Rescue of Female Infertility from the Loss of Cyclooxygenase-2 by Compensatory Up-regulation of Cyclooxygenase-1 Is a Function of Genetic Makeup

Wang

Tejada

et al. 2004

Journal of Biological Chemistry

114

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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.

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Section: Discussionmentioning

confidence: 99%

Rescue of Female Infertility from the Loss of Cyclooxygenase-2 by Compensatory Up-regulation of Cyclooxygenase-1 Is a Function of Genetic Makeup

Wang

Tejada

et al. 2004

Journal of Biological Chemistry

114

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“…Use of the appropriate strain of animal model is important as well [18]. Genetic backgrounds of animal models determine the metabolic rate of a chemical, mediating how that chemical is absorbed, distributed, metabolized, and excreted among different species [19][20][21]. Ultimately, this may affect how sensitive strains are to the same chemical under the same exposure conditions [22].…”

Section: Introductionmentioning

confidence: 99%

Mouse Strain Does Not Influence the Overall Effects of Bisphenol A-Induced Toxicity in Adult Antral Follicles1

Peretz

Neese

Flaws

2013

Biology of Reproduction

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Bisphenol A (BPA) is an endocrine-disrupting chemical (EDC) widely used in common consumer products containing polycarbonate plastics and epoxy resins. Previous studies indicate that other EDCs have species-dependent effects. Furthermore, some EDCs are known to have different effects in different strains within the same species. Little information, however, is known about whether the effects of BPA on the ovary differ by strain. Previous studies have shown that BPA inhibits follicle growth, induces atresia, and inhibits steroidogenesis and expression of steroidogenic enzymes in antral follicles from adult FVB mice. Thus, this study was designed to expand previous work by testing the hypothesis that mouse strain may differentially affect the susceptibility of adult antral follicles to BPA-induced toxicity. To test this hypothesis, antral follicles were mechanically isolated from adult FVB, CD-1, and C57BL/6 mice, individually cultured for 6-120 h and treated with either vehicle control (dimethylsulfoxide) or various concentrations of BPA (1.0 μg/ml, 10 μg/ml, or 100 μg/ml). After culture, media were subjected to measurements of hormone production via ELISA, and follicles were subjected to real-time PCR for analysis of genes known to regulate steroidogenesis, the cell cycle, and atresia. Overall, BPA inhibited follicle growth and steroidogenesis in all tested strains, but CD-1 follicles were slightly more sensitive to BPA at early time points than FVB and C57BL/6 follicles. These data suggest that CD-1, FVB, and C57BL/6 mice can all be used to investigate the effects of BPA on ovarian follicles.

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“…Many aspects of reproduction and development vary depending on the mouse strain including spermatogenesis, hormone-induced ovulation rates, and susceptibility to breast cancer (Spearow & Barkley 1999, Spearow et al 1999a, 1999b, Davie et al 2007. Some strains, such as CD-1, have been selected for large litter size, and because of this other reproductive traits are coinherited (Taketo et al 1991).…”

Section: Introductionmentioning

confidence: 99%

Differences in oocyte development and estradiol sensitivity among mouse strains

et al. 2010

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Mouse oocytes develop in clusters of interconnected cells called germline cysts. Shortly after birth, the majority of cysts break apart and primordial follicles form, consisting of one oocyte surrounded by granulosa cells. Concurrently, oocyte number is reduced by two-thirds. Exposure of neonatal females to estrogenic compounds causes multiple oocyte follicles that are likely germline cysts that did not break down. Supporting this idea, estrogen disrupts cyst breakdown and may regulate normal oocyte development. Previously, the CD-1 strain was used to study cyst breakdown and oocyte survival, but it is unknown if there are differences in these processes in other mouse strains. It is also unknown if there are variations in estrogen sensitivity during oocyte development. Here, we examined neonatal oocyte development in FVB, C57BL/6, and F2 hybrid (Oct4-GFP) strains, and compared them with the CD-1 strain. We found variability in oocyte development among the four strains. We also investigated estrogen sensitivity differences, and found that C57BL/6 ovaries are more sensitive to estradiol than CD-1, FVB, or Oct4-GFP ovaries. Insight into differences in oocyte development will facilitate comparison of mice generated on different genetic backgrounds. Understanding variations in estrogen sensitivity will lead to better understanding of the risks of environmental estrogen exposure in humans.

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Genetic Control of Hormone-Induced Ovulation Rate in Mice1

Cited by 53 publications

References 28 publications

Rescue of Female Infertility from the Loss of Cyclooxygenase-2 by Compensatory Up-regulation of Cyclooxygenase-1 Is a Function of Genetic Makeup

Rescue of Female Infertility from the Loss of Cyclooxygenase-2 by Compensatory Up-regulation of Cyclooxygenase-1 Is a Function of Genetic Makeup

Mouse Strain Does Not Influence the Overall Effects of Bisphenol A-Induced Toxicity in Adult Antral Follicles1

Differences in oocyte development and estradiol sensitivity among mouse strains

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