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Impact of uteroplacental insufficiency on ovarian follicular pool in the rat

BACKGROUND: A low oxygen supply to the fetus causes intrauterine growth restriction and can affect gonadal development of the offspring, having a potential impact on fertility. We investigated histology and gene expression in the postnatal rat ovary after fetal hypoxia induced by uterine artery liga...

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Autores principales: Pampanini, Valentina, Jahnukainen, Kirsi, Sahlin, Lena, Germani, Daniela, Puglianiello, Antonella, Cianfarani, Stefano, Söder, Olle
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329190/
https://www.ncbi.nlm.nih.gov/pubmed/30630482
http://dx.doi.org/10.1186/s12958-019-0453-3
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author Pampanini, Valentina
Jahnukainen, Kirsi
Sahlin, Lena
Germani, Daniela
Puglianiello, Antonella
Cianfarani, Stefano
Söder, Olle
author_facet Pampanini, Valentina
Jahnukainen, Kirsi
Sahlin, Lena
Germani, Daniela
Puglianiello, Antonella
Cianfarani, Stefano
Söder, Olle
author_sort Pampanini, Valentina
collection PubMed
description BACKGROUND: A low oxygen supply to the fetus causes intrauterine growth restriction and can affect gonadal development of the offspring, having a potential impact on fertility. We investigated histology and gene expression in the postnatal rat ovary after fetal hypoxia induced by uterine artery ligation. METHODS: Sprague-Dawley rats underwent uterine artery ligation at day 19 of gestation. Offspring were sacrificed at 5, 20 and 40 days post-partum. Follicles were counted and classified in hematoxylin-eosin stained sections. Gene expression of 90 genes was analyzed by TaqMan® Low Density Array. RESULTS: A significantly lower number of total and primordial follicles was detected in 20 days post-partum intrauterine growth restricted animals. Follicle density was not different at 40 days post-partum, suggesting that compensatory mechanisms occurred during the pre-pubertal window. Uterine artery ligation modified the expression of 24 genes involved in different cellular functions, among which proliferation, apoptosis and metabolism. CONCLUSION: Ovarian follicle pool was affected by fetal hypoxia in early life, but this effect did not persist in puberty. Genes involved in cellular processes were affected at all ages, potentially implying long-term genetic alterations. Further analyses are needed to elucidate later effects of fetal hypoxia on ovarian function and fertility. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12958-019-0453-3) contains supplementary material, which is available to authorized users.
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spelling pubmed-63291902019-01-16 Impact of uteroplacental insufficiency on ovarian follicular pool in the rat Pampanini, Valentina Jahnukainen, Kirsi Sahlin, Lena Germani, Daniela Puglianiello, Antonella Cianfarani, Stefano Söder, Olle Reprod Biol Endocrinol Research BACKGROUND: A low oxygen supply to the fetus causes intrauterine growth restriction and can affect gonadal development of the offspring, having a potential impact on fertility. We investigated histology and gene expression in the postnatal rat ovary after fetal hypoxia induced by uterine artery ligation. METHODS: Sprague-Dawley rats underwent uterine artery ligation at day 19 of gestation. Offspring were sacrificed at 5, 20 and 40 days post-partum. Follicles were counted and classified in hematoxylin-eosin stained sections. Gene expression of 90 genes was analyzed by TaqMan® Low Density Array. RESULTS: A significantly lower number of total and primordial follicles was detected in 20 days post-partum intrauterine growth restricted animals. Follicle density was not different at 40 days post-partum, suggesting that compensatory mechanisms occurred during the pre-pubertal window. Uterine artery ligation modified the expression of 24 genes involved in different cellular functions, among which proliferation, apoptosis and metabolism. CONCLUSION: Ovarian follicle pool was affected by fetal hypoxia in early life, but this effect did not persist in puberty. Genes involved in cellular processes were affected at all ages, potentially implying long-term genetic alterations. Further analyses are needed to elucidate later effects of fetal hypoxia on ovarian function and fertility. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12958-019-0453-3) contains supplementary material, which is available to authorized users. BioMed Central 2019-01-10 /pmc/articles/PMC6329190/ /pubmed/30630482 http://dx.doi.org/10.1186/s12958-019-0453-3 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Pampanini, Valentina
Jahnukainen, Kirsi
Sahlin, Lena
Germani, Daniela
Puglianiello, Antonella
Cianfarani, Stefano
Söder, Olle
Impact of uteroplacental insufficiency on ovarian follicular pool in the rat
title Impact of uteroplacental insufficiency on ovarian follicular pool in the rat
title_full Impact of uteroplacental insufficiency on ovarian follicular pool in the rat
title_fullStr Impact of uteroplacental insufficiency on ovarian follicular pool in the rat
title_full_unstemmed Impact of uteroplacental insufficiency on ovarian follicular pool in the rat
title_short Impact of uteroplacental insufficiency on ovarian follicular pool in the rat
title_sort impact of uteroplacental insufficiency on ovarian follicular pool in the rat
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329190/
https://www.ncbi.nlm.nih.gov/pubmed/30630482
http://dx.doi.org/10.1186/s12958-019-0453-3
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