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Deciphering reproductive aging in women using a NOD/SCID mouse model for distinct physiological ovarian phenotypes

Female fertility is negatively correlated with age, with noticeable declines in oocyte quantity and quality until menopause. To understand this physiological process and evaluate human approaches for treating age-related infertility, preclinical studies in appropriate animal models are needed. Thus,...

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Autores principales: Marchante, María, Ramirez-Martin, Noelia, Buigues, Anna, Martinez, Jessica, Pellicer, Nuria, Pellicer, Antonio, Herraiz, Sonia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10637815/
https://www.ncbi.nlm.nih.gov/pubmed/37847151
http://dx.doi.org/10.18632/aging.205086
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author Marchante, María
Ramirez-Martin, Noelia
Buigues, Anna
Martinez, Jessica
Pellicer, Nuria
Pellicer, Antonio
Herraiz, Sonia
author_facet Marchante, María
Ramirez-Martin, Noelia
Buigues, Anna
Martinez, Jessica
Pellicer, Nuria
Pellicer, Antonio
Herraiz, Sonia
author_sort Marchante, María
collection PubMed
description Female fertility is negatively correlated with age, with noticeable declines in oocyte quantity and quality until menopause. To understand this physiological process and evaluate human approaches for treating age-related infertility, preclinical studies in appropriate animal models are needed. Thus, we aimed to characterize an immunodeficient physiological aging mouse model displaying ovarian characteristics of different stages during women's reproductive life. NOD/SCID mice of different ages (8-, 28-, and 36–40-week-old) were employed to mimic ovarian phenotypes of young, Advanced Maternal Age (AMA), and old women (~18–20-, ~36–38-, and >45-years-old, respectively). Mice were stimulated, mated, and sacrificed to recover oocytes and embryos. Then, ovarian reserve, follicular growth, ovarian stroma, mitochondrial dysfunction, and proteomic profiles were assessed. Age-matched C57BL/6 mice were employed to cross-validate the reproductive outcomes. The quantity and quality of oocytes were decreased in AMA and Old mice. These age-related effects associated spindle and chromosome abnormalities, along with decreased developmental competence to blastocyst stage. Old mice had less follicles, impaired follicle activation and growth, an ovarian stroma inconducive to growth, and increased mitochondrial dysfunctions. Proteomic analysis corroborated these histological findings. Based on that, NOD/SCID mice can be used to model different ovarian aging phenotypes and potentially test human anti-aging treatments.
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spelling pubmed-106378152023-11-15 Deciphering reproductive aging in women using a NOD/SCID mouse model for distinct physiological ovarian phenotypes Marchante, María Ramirez-Martin, Noelia Buigues, Anna Martinez, Jessica Pellicer, Nuria Pellicer, Antonio Herraiz, Sonia Aging (Albany NY) Research Paper Female fertility is negatively correlated with age, with noticeable declines in oocyte quantity and quality until menopause. To understand this physiological process and evaluate human approaches for treating age-related infertility, preclinical studies in appropriate animal models are needed. Thus, we aimed to characterize an immunodeficient physiological aging mouse model displaying ovarian characteristics of different stages during women's reproductive life. NOD/SCID mice of different ages (8-, 28-, and 36–40-week-old) were employed to mimic ovarian phenotypes of young, Advanced Maternal Age (AMA), and old women (~18–20-, ~36–38-, and >45-years-old, respectively). Mice were stimulated, mated, and sacrificed to recover oocytes and embryos. Then, ovarian reserve, follicular growth, ovarian stroma, mitochondrial dysfunction, and proteomic profiles were assessed. Age-matched C57BL/6 mice were employed to cross-validate the reproductive outcomes. The quantity and quality of oocytes were decreased in AMA and Old mice. These age-related effects associated spindle and chromosome abnormalities, along with decreased developmental competence to blastocyst stage. Old mice had less follicles, impaired follicle activation and growth, an ovarian stroma inconducive to growth, and increased mitochondrial dysfunctions. Proteomic analysis corroborated these histological findings. Based on that, NOD/SCID mice can be used to model different ovarian aging phenotypes and potentially test human anti-aging treatments. Impact Journals 2023-10-16 /pmc/articles/PMC10637815/ /pubmed/37847151 http://dx.doi.org/10.18632/aging.205086 Text en Copyright: © 2023 Marchante et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Marchante, María
Ramirez-Martin, Noelia
Buigues, Anna
Martinez, Jessica
Pellicer, Nuria
Pellicer, Antonio
Herraiz, Sonia
Deciphering reproductive aging in women using a NOD/SCID mouse model for distinct physiological ovarian phenotypes
title Deciphering reproductive aging in women using a NOD/SCID mouse model for distinct physiological ovarian phenotypes
title_full Deciphering reproductive aging in women using a NOD/SCID mouse model for distinct physiological ovarian phenotypes
title_fullStr Deciphering reproductive aging in women using a NOD/SCID mouse model for distinct physiological ovarian phenotypes
title_full_unstemmed Deciphering reproductive aging in women using a NOD/SCID mouse model for distinct physiological ovarian phenotypes
title_short Deciphering reproductive aging in women using a NOD/SCID mouse model for distinct physiological ovarian phenotypes
title_sort deciphering reproductive aging in women using a nod/scid mouse model for distinct physiological ovarian phenotypes
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10637815/
https://www.ncbi.nlm.nih.gov/pubmed/37847151
http://dx.doi.org/10.18632/aging.205086
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