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Published on: August 11, 2023
Genetic contributions of the endothelial nitric oxide synthase gene to ovulation and menopause in a mouse model
C Tempfer1, R M Moreno, W E O'Brien
1University of Vienna, Vienna, Austria. clemens.tempfer@akh-wien.ac.at
Objective:
To investigate the influence of the endothelial nitric oxide synthase gene (Nos3) on ovulatory capacity and reproductive senescence.
Design:
Prospective, controlled study.
Setting:
Academic research institution.
Subject(S):
Laboratory mice with targeted mutagenesis of Nos3.
Intervention(S):
Hyperstimulation protocol, oocyte culture, and ovarian histology using wild-type (Nos3(+/+); n = 20), heterozygous (Nos3(+/m); n = 39), and homozygous deficient (Nos3(m/m); n = 11) female mice; observation of reproductive outcomes.
Main Outcome Measure(S):
Number and survival of oocytes; onset of menarche and menopause.
Result(S):
The mean number of superovulated oocytes (18 +/- 36 vs. 41 +/- 4) and the 48-hour overall survival rate of embryos (65% vs. 81%) were significantly reduced for Nos3(m/m) female mice compared with Nos3(+/+) female mice. Nos3(m/m) females showed a significantly reduced number and size of antral follicles and corpora lutea compared with wild-type controls. Compared with Nos3(+/m) x Nos3(+/m) breedings, Nos3(m/m) x Nos3(m/m) breedings showed a higher female age at first litter (76.2 +/- 10.3 vs. 107.8 +/- 26.6 days), fewer litters (10.5 +/- 3.6 vs. 7. 8 +/- 4.2), and a lower female age at reproductive senescence (400.2 +/- 64.5 vs. 332.1 +/- 27.4 days), respectively.
Conclusion(S):
Our data suggest that Nos3 deficiency is associated with reduced ovulatory capacity and impaired early embryonic viability and that it influences the onset of menarche and menopause.
Insights
Endothelial nitric oxide synthase gene (Nos3) deficiency in female mice significantly reduces ovulatory capacity and embryo survival. Nos3 deficiency also impacts reproductive senescence, affecting the timing of reproductive milestones.
Area of Science:
- Reproductive biology
- Genetics
- Molecular biology
Background:
- Endothelial nitric oxide synthase (Nos3) plays a crucial role in vascular function and reproductive processes.
- Understanding the genetic influence of Nos3 on female reproduction is essential for reproductive health research.
Purpose of the Study:
- To investigate the impact of the endothelial nitric oxide synthase gene (Nos3) on ovulatory capacity and reproductive senescence in a mouse model.
- To determine the relationship between Nos3 deficiency and key reproductive outcomes.
Main Methods:
- A prospective, controlled study was conducted using laboratory mice with targeted mutagenesis of the Nos3 gene.
- Mice included wild-type (Nos3(+/+)), heterozygous (Nos3(+/m)), and homozygous deficient (Nos3(m/m)) females.
- Reproductive outcomes were assessed through hyperstimulation protocols, oocyte culture, ovarian histology, and observation of reproductive milestones.
Main Results:
- Nos3-deficient (Nos3(m/m)) female mice exhibited significantly reduced numbers of superovulated oocytes and lower embryonic survival rates compared to wild-type controls.
- Ovarian histology revealed fewer and smaller antral follicles and corpora lutea in Nos3(m/m) mice.
- Breeding studies showed that Nos3 deficiency led to a later age at first litter, fewer litters, and an earlier age at reproductive senescence.
Conclusions:
- Nos3 deficiency is associated with diminished ovulatory capacity and impaired early embryonic viability.
- The genetic influence of Nos3 extends to the regulation of reproductive senescence, affecting the onset of reproductive milestones like menarche and menopause.
