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Blood Cell Mitochondrial DNA Content and Premature Ovarian Aging

Primary ovarian insufficiency (POI) is a critical fertility defect characterized by an anticipated and silent impairment of the follicular reserve, but its pathogenesis is largely unexplained. The frequent maternal inheritance of POI together with a remarkable dependence of ovarian folliculogenesis...

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Autores principales: Bonomi, Marco, Somigliana, Edgardo, Cacciatore, Chiara, Busnelli, Marta, Rossetti, Raffaella, Bonetti, Silvia, Paffoni, Alessio, Mari, Daniela, Ragni, Guido, Persani, Luca
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3411770/
https://www.ncbi.nlm.nih.gov/pubmed/22879975
http://dx.doi.org/10.1371/journal.pone.0042423
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author Bonomi, Marco
Somigliana, Edgardo
Cacciatore, Chiara
Busnelli, Marta
Rossetti, Raffaella
Bonetti, Silvia
Paffoni, Alessio
Mari, Daniela
Ragni, Guido
Persani, Luca
author_facet Bonomi, Marco
Somigliana, Edgardo
Cacciatore, Chiara
Busnelli, Marta
Rossetti, Raffaella
Bonetti, Silvia
Paffoni, Alessio
Mari, Daniela
Ragni, Guido
Persani, Luca
author_sort Bonomi, Marco
collection PubMed
description Primary ovarian insufficiency (POI) is a critical fertility defect characterized by an anticipated and silent impairment of the follicular reserve, but its pathogenesis is largely unexplained. The frequent maternal inheritance of POI together with a remarkable dependence of ovarian folliculogenesis upon mitochondrial biogenesis and bioenergetics suggested the possible involvement of a generalized mitochondrial defect. Here, we verified the existence of a significant correlation between blood and ovarian mitochondrial DNA (mtDNA) content in a group of women undergoing ovarian hyperstimulation (OH), and then aimed to verify whether mtDNA content was significantly altered in the blood cells of POI women. We recruited 101 women with an impaired ovarian reserve: 59 women with premature ovarian failure (POF) and 42 poor responders (PR) to OH. A Taqman copy number assay revealed a significant mtDNA depletion (P<0.001) in both POF and PR women in comparison with 43 women of similar age and intact ovarian reserve, or 53 very old women with a previous physiological menopause. No pathogenic variations in the mitochondrial DNA polymerase γ (POLG) gene were detected in 57 POF or PR women with low blood mtDNA content. In conclusion, blood cell mtDNA depletion is a frequent finding among women with premature ovarian aging, suggesting that a still undetermined but generalized mitochondrial defect may frequently predispose to POI which could then be considered a form of anticipated aging in which the ovarian defect may represent the first manifestation. The determination of mtDNA content in blood may become an useful tool for the POI risk prediction.
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spelling pubmed-34117702012-08-09 Blood Cell Mitochondrial DNA Content and Premature Ovarian Aging Bonomi, Marco Somigliana, Edgardo Cacciatore, Chiara Busnelli, Marta Rossetti, Raffaella Bonetti, Silvia Paffoni, Alessio Mari, Daniela Ragni, Guido Persani, Luca PLoS One Research Article Primary ovarian insufficiency (POI) is a critical fertility defect characterized by an anticipated and silent impairment of the follicular reserve, but its pathogenesis is largely unexplained. The frequent maternal inheritance of POI together with a remarkable dependence of ovarian folliculogenesis upon mitochondrial biogenesis and bioenergetics suggested the possible involvement of a generalized mitochondrial defect. Here, we verified the existence of a significant correlation between blood and ovarian mitochondrial DNA (mtDNA) content in a group of women undergoing ovarian hyperstimulation (OH), and then aimed to verify whether mtDNA content was significantly altered in the blood cells of POI women. We recruited 101 women with an impaired ovarian reserve: 59 women with premature ovarian failure (POF) and 42 poor responders (PR) to OH. A Taqman copy number assay revealed a significant mtDNA depletion (P<0.001) in both POF and PR women in comparison with 43 women of similar age and intact ovarian reserve, or 53 very old women with a previous physiological menopause. No pathogenic variations in the mitochondrial DNA polymerase γ (POLG) gene were detected in 57 POF or PR women with low blood mtDNA content. In conclusion, blood cell mtDNA depletion is a frequent finding among women with premature ovarian aging, suggesting that a still undetermined but generalized mitochondrial defect may frequently predispose to POI which could then be considered a form of anticipated aging in which the ovarian defect may represent the first manifestation. The determination of mtDNA content in blood may become an useful tool for the POI risk prediction. Public Library of Science 2012-08-03 /pmc/articles/PMC3411770/ /pubmed/22879975 http://dx.doi.org/10.1371/journal.pone.0042423 Text en © 2012 Bonomi et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Bonomi, Marco
Somigliana, Edgardo
Cacciatore, Chiara
Busnelli, Marta
Rossetti, Raffaella
Bonetti, Silvia
Paffoni, Alessio
Mari, Daniela
Ragni, Guido
Persani, Luca
Blood Cell Mitochondrial DNA Content and Premature Ovarian Aging
title Blood Cell Mitochondrial DNA Content and Premature Ovarian Aging
title_full Blood Cell Mitochondrial DNA Content and Premature Ovarian Aging
title_fullStr Blood Cell Mitochondrial DNA Content and Premature Ovarian Aging
title_full_unstemmed Blood Cell Mitochondrial DNA Content and Premature Ovarian Aging
title_short Blood Cell Mitochondrial DNA Content and Premature Ovarian Aging
title_sort blood cell mitochondrial dna content and premature ovarian aging
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3411770/
https://www.ncbi.nlm.nih.gov/pubmed/22879975
http://dx.doi.org/10.1371/journal.pone.0042423
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