Journal
ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY
Volume 290, Issue 1, Pages 59-64Publisher
WILEY
DOI: 10.1002/ar.20409
Keywords
P53 knockout; ovulation; mice
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Funding
- NCRR NIH HHS [P20RR016474, P20 RR016474-08, P20 RR016474] Funding Source: Medline
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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. Anat Rec, 290:59-64, 2007. (c) 2006 Wiley-Liss, Inc.
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