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Updated: Jan 19, 2026
Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome
Published on: July 5, 2024
Inducible and endothelial nitric oxide synthase: genetic background affects ovulation in mice
Lukas A Hefler1, Anthony R Gregg
1Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, Texas 77030, USA.
Objective:
Inducible nitric oxide synthase (NOS) and endothelial NOS are involved in female reproductive physiology. We sought to investigate the influence of the inducible (Nos2) and endothelial (Nos3) NOS genes as a function of genetic background on ovulatory capacity and early embryonic development in a mouse model.
Design:
Observational study of genetically altered mice and their response to a superovulation protocol.
Setting:
Academic research institution.
Animals:
Wild-type mice and mice deficient for Nos2 or Nos3 were bred to C57BL/6J and 129/Sv genetic backgrounds.
Intervention(S):
Superovulation protocol, oocyte culture.
Main Outcome Measure(S):
Number of oocytes harvested, early embryonic development of zygotes, evaluation of ovarian histology.
Result(S):
The mean number of oocytes was significantly reduced in Nos3 deficient mice on a C57BL/6J background compared with controls. Oocytes deficient for Nos3 on a C57BL/6J background also showed reduced progression to two-cell stage embryos after 24 hours, two-cell stage embryos to blastocyst stage embryos, and survival to 48 hours. Those effects were distinctly absent in mice deficient for Nos3 on a 129/Sv background and in mice deficient for Nos2 on either genetic background.
Conclusion(S):
Our data show that disruption of Nos2 had no effect on ovulation in our mice. The negative effect of Nos3 deficiency on ovulatory capacity and early embryonic development is modulated by genetic background. This suggests a role for strain-specific modifier genes in these processes.
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