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FSH regulates RA signaling to commit spermatogonia into differentiation pathway and meiosis
BACKGROUND: Spermatogenesis is a complex process that is controlled by interactions between germ cells and somatic cells. The commitment of undifferentiated spermatogonia to differentiating spermatogonia and normal spermatogenesis requires the action of gonadotropins. Additionally, numerous studies...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7789255/ https://www.ncbi.nlm.nih.gov/pubmed/33407539 http://dx.doi.org/10.1186/s12958-020-00686-w |
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author | Khanehzad, Maryam Abbaszadeh, Roya Holakuyee, Marzieh Modarressi, Mohammad Hossein Nourashrafeddin, Seyed Mehdi |
author_facet | Khanehzad, Maryam Abbaszadeh, Roya Holakuyee, Marzieh Modarressi, Mohammad Hossein Nourashrafeddin, Seyed Mehdi |
author_sort | Khanehzad, Maryam |
collection | PubMed |
description | BACKGROUND: Spermatogenesis is a complex process that is controlled by interactions between germ cells and somatic cells. The commitment of undifferentiated spermatogonia to differentiating spermatogonia and normal spermatogenesis requires the action of gonadotropins. Additionally, numerous studies revealed the role of retinoic acid signaling in induction of germ cell differentiation and meiosis entry. MAIN TEXT: Recent studies have shown that expression of several RA signaling molecules including Rdh10, Aldh1a2, Crabp1/2 are influenced by changes in gonadotropin levels. Components of signaling pathways that are regulated by FSH signaling such as GDNF, Sohlh1/2, c-Kit, DMRT, BMP4 and NRGs along with transcription factors that are important for proliferation and differentiation of spermatogonia are also affected by retinoic acid signaling. CONCLUSION: According to all studies that demonstrate the interface between FSH and RA signaling, we suggest that RA may trigger spermatogonia differentiation and initiation of meiosis through regulation by FSH signaling in testis. Therefore, to the best of our knowledge, this is the first time that the correlation between FSH and RA signaling in spermatogenesis is highlighted. |
format | Online Article Text |
id | pubmed-7789255 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-77892552021-01-07 FSH regulates RA signaling to commit spermatogonia into differentiation pathway and meiosis Khanehzad, Maryam Abbaszadeh, Roya Holakuyee, Marzieh Modarressi, Mohammad Hossein Nourashrafeddin, Seyed Mehdi Reprod Biol Endocrinol Review BACKGROUND: Spermatogenesis is a complex process that is controlled by interactions between germ cells and somatic cells. The commitment of undifferentiated spermatogonia to differentiating spermatogonia and normal spermatogenesis requires the action of gonadotropins. Additionally, numerous studies revealed the role of retinoic acid signaling in induction of germ cell differentiation and meiosis entry. MAIN TEXT: Recent studies have shown that expression of several RA signaling molecules including Rdh10, Aldh1a2, Crabp1/2 are influenced by changes in gonadotropin levels. Components of signaling pathways that are regulated by FSH signaling such as GDNF, Sohlh1/2, c-Kit, DMRT, BMP4 and NRGs along with transcription factors that are important for proliferation and differentiation of spermatogonia are also affected by retinoic acid signaling. CONCLUSION: According to all studies that demonstrate the interface between FSH and RA signaling, we suggest that RA may trigger spermatogonia differentiation and initiation of meiosis through regulation by FSH signaling in testis. Therefore, to the best of our knowledge, this is the first time that the correlation between FSH and RA signaling in spermatogenesis is highlighted. BioMed Central 2021-01-07 /pmc/articles/PMC7789255/ /pubmed/33407539 http://dx.doi.org/10.1186/s12958-020-00686-w Text en © The Author(s) 2021 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data. |
spellingShingle | Review Khanehzad, Maryam Abbaszadeh, Roya Holakuyee, Marzieh Modarressi, Mohammad Hossein Nourashrafeddin, Seyed Mehdi FSH regulates RA signaling to commit spermatogonia into differentiation pathway and meiosis |
title | FSH regulates RA signaling to commit spermatogonia into differentiation pathway and meiosis |
title_full | FSH regulates RA signaling to commit spermatogonia into differentiation pathway and meiosis |
title_fullStr | FSH regulates RA signaling to commit spermatogonia into differentiation pathway and meiosis |
title_full_unstemmed | FSH regulates RA signaling to commit spermatogonia into differentiation pathway and meiosis |
title_short | FSH regulates RA signaling to commit spermatogonia into differentiation pathway and meiosis |
title_sort | fsh regulates ra signaling to commit spermatogonia into differentiation pathway and meiosis |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7789255/ https://www.ncbi.nlm.nih.gov/pubmed/33407539 http://dx.doi.org/10.1186/s12958-020-00686-w |
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