Rapid ovarian transcript changes during the onset of premature ovarian insufficiency in a mouse model

Premature ovarian insufficiency (POI) affects 1-3% of women under 40 years of age. The identified causes are highly heterogeneous, and 70% of the cases are idiopathic. The ovarian manifestation varies from a variable population of follicles that fail to develop (follicular POI) to the absence of fol...

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Main Authors: Heidy Kaune, Juan F Montiel, Mark Fenwick, Suzannah A Williams
Format: Article
Language:English
Published: Bioscientifica 2022-09-01
Series:Reproduction and Fertility
Subjects:
Online Access:https://raf.bioscientifica.com/view/journals/raf/3/3/RAF-22-0036.xml
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author Heidy Kaune
Juan F Montiel
Mark Fenwick
Suzannah A Williams
author_facet Heidy Kaune
Juan F Montiel
Mark Fenwick
Suzannah A Williams
author_sort Heidy Kaune
collection DOAJ
description Premature ovarian insufficiency (POI) affects 1-3% of women under 40 years of age. The identified causes are highly heterogeneous, and 70% of the cases are idiopathic. The ovarian manifestation varies from a variable population of follicles that fail to develop (follicular POI) to the absence of follicles (afollicular POI) with a transition from one to the other over time. Previously, we have described a mouse model of POI that results from an oocyte-specific deletion of N- and O-glycans; Double Mutant (DM). DM females produce only one litter before undergoing POI due to ovarian dysfunction. In this study, we have characterised the gene expression profile of prepuberal (3 weeks), fertile (6 weeks) and infertile (9 weeks) DM ovaries. Up-regulation of cathepsin K (Ctsk, with unknown ovarian function) seems to trigger transcriptional changes in DM ovaries. Significant transcriptional changes then occur rapidly, associated with morphophysiological changes displayed by DM mice throughout the onset of POI. We identified genetic pathways such as extracellular matrix and immune response as candidates for the onset of POI in DM females. Remarkably, DM mice and POI women share a set of differentially expressed genes, including a functionally and co-expressed network of Mcm (minichromosome maintenance proteins) family members. The transcriptomic profile of the DM mouse model provides novel insight into the aetiology of POI.
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spelling doaj.art-d521302eddcf4e72a6f55645762b99a12022-12-22T02:03:30ZengBioscientificaReproduction and Fertility2633-83862022-09-0133173186https://doi.org/10.1530/RAF-22-0036Rapid ovarian transcript changes during the onset of premature ovarian insufficiency in a mouse modelHeidy Kaune0Juan F Montiel1Mark Fenwick2Suzannah A Williams3Laboratory of Reproduction, Centre for Biomedical Research, Faculty of Medicine, Universidad Diego Portales, Santiago, Chile; Program of Ethics and Public Policies in Human Reproduction, Universidad Diego Portales, Santiago, Chile Laboratory of Integrative Neuroscience, Centre for Biomedical Research, Faculty of Medicine, Universidad Diego Portales, Santiago, ChileAcademic Unit of Reproductive and Developmental Medicine, University of Sheffield, Sheffield, UKNuffield Department of Women’s and Reproductive Health, Women’s Centre, John Radcliffe Hospital, University of Oxford, Oxford, UKPremature ovarian insufficiency (POI) affects 1-3% of women under 40 years of age. The identified causes are highly heterogeneous, and 70% of the cases are idiopathic. The ovarian manifestation varies from a variable population of follicles that fail to develop (follicular POI) to the absence of follicles (afollicular POI) with a transition from one to the other over time. Previously, we have described a mouse model of POI that results from an oocyte-specific deletion of N- and O-glycans; Double Mutant (DM). DM females produce only one litter before undergoing POI due to ovarian dysfunction. In this study, we have characterised the gene expression profile of prepuberal (3 weeks), fertile (6 weeks) and infertile (9 weeks) DM ovaries. Up-regulation of cathepsin K (Ctsk, with unknown ovarian function) seems to trigger transcriptional changes in DM ovaries. Significant transcriptional changes then occur rapidly, associated with morphophysiological changes displayed by DM mice throughout the onset of POI. We identified genetic pathways such as extracellular matrix and immune response as candidates for the onset of POI in DM females. Remarkably, DM mice and POI women share a set of differentially expressed genes, including a functionally and co-expressed network of Mcm (minichromosome maintenance proteins) family members. The transcriptomic profile of the DM mouse model provides novel insight into the aetiology of POI.https://raf.bioscientifica.com/view/journals/raf/3/3/RAF-22-0036.xmlovaryfertilityoocyte
spellingShingle Heidy Kaune
Juan F Montiel
Mark Fenwick
Suzannah A Williams
Rapid ovarian transcript changes during the onset of premature ovarian insufficiency in a mouse model
Reproduction and Fertility
ovary
fertility
oocyte
title Rapid ovarian transcript changes during the onset of premature ovarian insufficiency in a mouse model
title_full Rapid ovarian transcript changes during the onset of premature ovarian insufficiency in a mouse model
title_fullStr Rapid ovarian transcript changes during the onset of premature ovarian insufficiency in a mouse model
title_full_unstemmed Rapid ovarian transcript changes during the onset of premature ovarian insufficiency in a mouse model
title_short Rapid ovarian transcript changes during the onset of premature ovarian insufficiency in a mouse model
title_sort rapid ovarian transcript changes during the onset of premature ovarian insufficiency in a mouse model
topic ovary
fertility
oocyte
url https://raf.bioscientifica.com/view/journals/raf/3/3/RAF-22-0036.xml
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AT suzannahawilliams rapidovariantranscriptchangesduringtheonsetofprematureovarianinsufficiencyinamousemodel