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Steroidal but not embryonic regulation of mucin 1 expression in bovine endometrium

In cow herd management, inadequate embryo implantation leads to pregnancy loss and causes severe economic losses. Thus, it is crucial to understand the molecular mechanisms underlying endometrial receptivity and subsequent embryo implantation. Transmembrane glycocalyx mucin 1 (MUC1) has a large and...

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Autores principales: KUBOTA, Kaiyu, MIWA, Masafumi, HAYASHI, Ken-Go, HOSOE, Misa, SAKATANI, Miki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Society for Reproduction and Development 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8668378/
https://www.ncbi.nlm.nih.gov/pubmed/34645736
http://dx.doi.org/10.1262/jrd.2021-087
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author KUBOTA, Kaiyu
MIWA, Masafumi
HAYASHI, Ken-Go
HOSOE, Misa
SAKATANI, Miki
author_facet KUBOTA, Kaiyu
MIWA, Masafumi
HAYASHI, Ken-Go
HOSOE, Misa
SAKATANI, Miki
author_sort KUBOTA, Kaiyu
collection PubMed
description In cow herd management, inadequate embryo implantation leads to pregnancy loss and causes severe economic losses. Thus, it is crucial to understand the molecular mechanisms underlying endometrial receptivity and subsequent embryo implantation. Transmembrane glycocalyx mucin 1 (MUC1) has a large and highly glycosylated extracellular domain known to inhibit embryo implantation via steric hindrance. The role of MUC1 in the bovine endometrium remains to be explored. Herein, we used simple but reliable in vivo and in vitro experiments to investigate the expression and regulation of MUC1 in the bovine endometrium. MUC1 gene expression was analyzed in endometrial epithelial cells collected by the cytobrush technique using reverse transcription-quantitative polymerase chain reaction. MUC1 protein expression was evaluated by immunohistochemical analysis of endometrial samples collected from slaughtered cows. We used an in vitro cell culture model to study the regulation of MUC1 expression by treating cells with sex steroidal hormones or co-culturing cells with a blastocyst. The results revealed that MUC1 was expressed and localized to the apical surface of luminal epithelial cells in the bovine endometrium. MUC1 expression disappeared during the luteal phase of the estrous cycle and during pregnancy. 17β-estradiol induced MUC1 expression, whereas progesterone inhibited its increase and co-culturing with blastocysts did not affect the expression. A long postpartum interval is a known risk factor for reduced fertility, and MUC1 expression was higher in this compromised condition. Our results demonstrated the MUC1 regulation by steroid hormones in bovine endometrium for embryo implantation, and we observed a negative correlation between MUC1 expression and fertility.
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spelling pubmed-86683782021-12-17 Steroidal but not embryonic regulation of mucin 1 expression in bovine endometrium KUBOTA, Kaiyu MIWA, Masafumi HAYASHI, Ken-Go HOSOE, Misa SAKATANI, Miki J Reprod Dev Original Article In cow herd management, inadequate embryo implantation leads to pregnancy loss and causes severe economic losses. Thus, it is crucial to understand the molecular mechanisms underlying endometrial receptivity and subsequent embryo implantation. Transmembrane glycocalyx mucin 1 (MUC1) has a large and highly glycosylated extracellular domain known to inhibit embryo implantation via steric hindrance. The role of MUC1 in the bovine endometrium remains to be explored. Herein, we used simple but reliable in vivo and in vitro experiments to investigate the expression and regulation of MUC1 in the bovine endometrium. MUC1 gene expression was analyzed in endometrial epithelial cells collected by the cytobrush technique using reverse transcription-quantitative polymerase chain reaction. MUC1 protein expression was evaluated by immunohistochemical analysis of endometrial samples collected from slaughtered cows. We used an in vitro cell culture model to study the regulation of MUC1 expression by treating cells with sex steroidal hormones or co-culturing cells with a blastocyst. The results revealed that MUC1 was expressed and localized to the apical surface of luminal epithelial cells in the bovine endometrium. MUC1 expression disappeared during the luteal phase of the estrous cycle and during pregnancy. 17β-estradiol induced MUC1 expression, whereas progesterone inhibited its increase and co-culturing with blastocysts did not affect the expression. A long postpartum interval is a known risk factor for reduced fertility, and MUC1 expression was higher in this compromised condition. Our results demonstrated the MUC1 regulation by steroid hormones in bovine endometrium for embryo implantation, and we observed a negative correlation between MUC1 expression and fertility. The Society for Reproduction and Development 2021-10-14 2021-12 /pmc/articles/PMC8668378/ /pubmed/34645736 http://dx.doi.org/10.1262/jrd.2021-087 Text en ©2021 Society for Reproduction and Development https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. (CC-BY-NC-ND 4.0: https://creativecommons.org/licenses/by-nc-nd/4.0/)
spellingShingle Original Article
KUBOTA, Kaiyu
MIWA, Masafumi
HAYASHI, Ken-Go
HOSOE, Misa
SAKATANI, Miki
Steroidal but not embryonic regulation of mucin 1 expression in bovine endometrium
title Steroidal but not embryonic regulation of mucin 1 expression in bovine endometrium
title_full Steroidal but not embryonic regulation of mucin 1 expression in bovine endometrium
title_fullStr Steroidal but not embryonic regulation of mucin 1 expression in bovine endometrium
title_full_unstemmed Steroidal but not embryonic regulation of mucin 1 expression in bovine endometrium
title_short Steroidal but not embryonic regulation of mucin 1 expression in bovine endometrium
title_sort steroidal but not embryonic regulation of mucin 1 expression in bovine endometrium
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8668378/
https://www.ncbi.nlm.nih.gov/pubmed/34645736
http://dx.doi.org/10.1262/jrd.2021-087
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