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Normal Ovarian Function in Subfertile Mouse with IAmhr2-/ICre-Driven Ablation of IInsr/I and IIgf1r/I
Genes, 2024-05, Vol.15 (5)
[Peer Reviewed Journal]
COPYRIGHT 2024 MDPI AG ;ISSN: 2073-4425 ;EISSN: 2073-4425 ;DOI: 10.3390/genes15050616
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Title:
Normal Ovarian Function in Subfertile Mouse with IAmhr2-/ICre-Driven Ablation of IInsr/I and IIgf1r/I
Author:
Douglas, Jenna C
;
Sekulovski, Nikola
;
Arreola, Madison R
;
Oh, Yeongseok
;
Hayashi, Kanako
;
MacLean, James A
Subjects:
Insulin
;
Type 2 diabetes
Is Part Of:
Genes, 2024-05, Vol.15 (5)
Description:
Insulin receptor signaling promotes cell differentiation, proliferation, and growth which are essential for oocyte maturation, embryo implantation, endometrial decidualization, and placentation. The dysregulation of insulin signaling in women with metabolic syndromes including diabetes exhibits poor pregnancy outcomes that are poorly understood. We utilized the Cre/LoxP system to target the tissue-specific conditional ablation of insulin receptor (Insr) and insulin-like growth factor-1 receptor (Igf1r) using an anti-Mullerian hormone receptor 2 (Amhr2) Cre-driver which is active in ovarian granulosa and uterine stromal cells. Our long-term goal is to examine insulin-dependent molecular mechanisms that underlie diabetic pregnancy complications, and our conditional knockout models allow for such investigation without confounding effects of ligand identity, source and cross-reactivity, or global metabolic status within dams. Puberty occurred with normal timing in all conditional knockout models. Estrous cycles progressed normally in Insrd/d females but were briefly stalled in diestrus in Igf1rd/d and double receptor (DKO) mice. The expression of vital ovulatory genes (Lhcgr, Pgr, Ptgs2) was not significantly different in 12 h post-hCG superovulated ovaries in knockout mice. Antral follicles exhibited an elevated apoptosis of granulosa cells in Igf1rd/d and DKO mice. However, the distribution of ovarian follicle subtypes and subsequent ovulations was normal in all insulin receptor mutants compared to littermate controls. While ovulation was normal, all knockout lines were subfertile suggesting that the loss of insulin receptor signaling in the uterine stroma elicits implantation and decidualization defects responsible for subfertility in Amhr2-Cre-derived insulin receptor mutants.
Publisher:
MDPI AG
Language:
English
Identifier:
ISSN: 2073-4425
EISSN: 2073-4425
DOI: 10.3390/genes15050616
Source:
PubMed Central
ROAD: Directory of Open Access Scholarly Resources
ProQuest Central
DOAJ Directory of Open Access Journals
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