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Ovarian morphometrics in TP53-deficient mice
Brenda M Alexander1, Edward A Van Kirk, Leann M A Naughton
1Department of Animal Science, University of Wyoming, Laramie, Wyoming 82071, USA. balex@uwyo.edu
Abstract:
The objective of these investigations was to characterize ovarian responses to hormonal stimulation in TP53-deficient mice. TP53-deficient (KO) and wild-type (WT) mice were induced to ovulate with pregnant mare serum gonadotropin followed by human chorionic gonadotropin. Effect of estradiol on ovarian morphology was determined in induced and control mice implanted with estradiol-containing or placebo pellets. Blood was collected and mice were killed 7 days following implantation. Preserved ovaries were serially sectioned and stained. Numbers of follicles (all classifications) decreased with ovulation induction, but did not differ between WT and KO mice. Numbers of corpora lutea (CL) were less in ovulation-induced KO mice treated with estradiol compared to WT mice. Area of individual CL and serum concentrations of progesterone were greater in ovulation-induced KO mice given estradiol compared to WT mice. Ovulation-induced KO mice had more, larger hemorrhagic follicles than similarly treated WT mice, but hemorrhagic follicles were not influenced by estradiol. Proliferation of ovarian surface epithelial cells did not differ between KO and WT mice induced to ovulate and given estradiol. Ovaries from TP53 gene knockout mice (n = 4) induced to ovulate and given a 21-day estradiol implant three times over 58 days were observed for precursor lesions. There was no indication of precursor lesions in any TP53 KO or WT mouse. TP53 status did not influence recruitment of follicles, but TP53 deficiency hindered the ability of human chorionic gonadotropin to cause ovulation.
Insights
TP53 deficiency in mice reduced ovulation rates but increased corpus luteum size and progesterone levels when stimulated with hormones and estradiol. Estradiol did not affect hemorrhagic follicles or ovarian surface epithelial cell proliferation.
Area of Science:
- Reproductive biology
- Genetics
- Endocrinology
Background:
- The TP53 tumor suppressor gene plays a critical role in cellular responses to DNA damage.
- Understanding TP53
- s role in ovarian function is crucial for reproductive health and cancer research.
Purpose of the Study:
- To investigate the impact of TP53 deficiency on ovarian responses to hormonal stimulation.
- To determine the effect of estradiol on ovarian morphology and function in TP53-deficient mice.
Main Methods:
- Ovulation was induced in TP53-deficient (KO) and wild-type (WT) mice using pregnant mare serum gonadotropin and human chorionic gonadotropin.
- Estradiol
- 's effects were assessed using hormone implants and placebo controls.
- Ovarian morphology, follicle counts, corpora lutea (CL) analysis, and serum progesterone levels were evaluated.
Main Results:
- Ovulation induction decreased follicle numbers but did not differ between WT and KO mice.
- TP53 deficiency reduced the number of CL in estradiol-treated mice but increased individual CL area and progesterone levels.
- Hemorrhagic follicle counts were higher in KO mice, independent of estradiol treatment.
Conclusions:
- TP53 status influences ovulation rates and corpus luteum function in response to hormonal stimulation.
- While TP53 deficiency hinders ovulation, it may enhance certain aspects of corpus luteum development and progesterone production.
- No evidence of precursor lesions was observed in TP53-deficient ovaries, suggesting TP53 is not essential for preventing early tumorigenesis in this context.
