G protein-coupled estrogen receptor 1 inhibits the epithelial–mesenchymal transition of goat mammary epithelial cells via NF-κB signalling pathway
Zhao, Ying ; Yang, Zhenshan LU
; Miao, Yuyang
; Fan, Mingzhen
; Zhao, Xiaoe
; Wei, Qiang
and Ma, Baohua
(2021)
In Reproduction in Domestic Animals
56(8).
p.1137-1144
- Abstract
Mastitis is one of the most frequent clinical diseases in dairy animals. Epithelial cells undergoing epithelial–mesenchymal transition (EMT) promote the process of mastitis. Oestrogen deficiency is disadvantaged of many tissue inflammation and regeneration, while exogenous oestrogen treatment can reverse these effects. G protein-coupled estrogen receptor 1 (GPER1) is a membrane estrogen receptor. However, the potential effects of oestrogen via GPER1 on EMT in goat mammary epithelial cells (GMECs) are still unclear. Here, this study discovered that the activation of GPER1 by oestrogen could inhibit the EMT in GMECs via NF-κB signalling pathway. The activation of GPER1 by oestrogen inhibited the EMT accompanied by upregulation of... (More)
Mastitis is one of the most frequent clinical diseases in dairy animals. Epithelial cells undergoing epithelial–mesenchymal transition (EMT) promote the process of mastitis. Oestrogen deficiency is disadvantaged of many tissue inflammation and regeneration, while exogenous oestrogen treatment can reverse these effects. G protein-coupled estrogen receptor 1 (GPER1) is a membrane estrogen receptor. However, the potential effects of oestrogen via GPER1 on EMT in goat mammary epithelial cells (GMECs) are still unclear. Here, this study discovered that the activation of GPER1 by oestrogen could inhibit the EMT in GMECs via NF-κB signalling pathway. The activation of GPER1 by oestrogen inhibited the EMT accompanied by upregulation of E-cadherin and downregulation of N-cadherin and vimentin. Meanwhile, mRNA expression of transcription factors including Snail1 and ZEB1 was decreased. Further, like to oestrogen, GPER1 agonist G1 repressed the EMT progression. Conversely, GPER1 antagonist G15 reversed all these features induced by oestrogen. What's more, GPER1 silencing with shRNA promoted GMECs undergoing EMT. Additionally, oestrogen increased the phosphorylation of Erk1/2, which then decreased the phosphorylation and nuclear translocation of NF-κB, inhibiting the NF-κB signalling pathway activity. Taken, GPER1 may act as a suppressor through the regulation of EMT to prevent the development of mastitis.
(Less)
- author
- Zhao, Ying
; Yang, Zhenshan
LU
; Miao, Yuyang
; Fan, Mingzhen
; Zhao, Xiaoe
; Wei, Qiang
and Ma, Baohua
- publishing date
- 2021-08
- type
- Contribution to journal
- publication status
- published
- keywords
- epithelial-mesenchymal transition, G protein-coupled estrogen receptor 1, goat, mammary epithelial cells, oestrogen
- in
- Reproduction in Domestic Animals
- volume
- 56
- issue
- 8
- pages
- 1137 - 1144
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:34021926
- scopus:85107162359
- ISSN
- 0936-6768
- DOI
- 10.1111/rda.13957
- language
- English
- LU publication?
- no
- additional info
- Funding Information: This work was supported by the National Natural Science Foundation of China (31772818) and the Key Research and Development Program of Shaanxi (2018NY-023). We wish to thank Professor Yulin Chen (College of Animal Science and Technology, Northwest A&F University, China) for their technical assistance. Funding Information: This work was supported by the National Natural Science Foundation of China (31772818) and the Key Research and Development Program of Shaanxi (2018NY‐023). We wish to thank Professor Yulin Chen (College of Animal Science and Technology, Northwest A&F University, China) for their technical assistance. Publisher Copyright: © 2021 Wiley-VCH GmbH
- id
- cebe3e9f-3cd9-4432-8d73-cb10d6586609
- date added to LUP
- 2024-02-28 14:59:49
- date last changed
- 2024-06-18 21:17:00
@article{cebe3e9f-3cd9-4432-8d73-cb10d6586609,
abstract = {{<p>Mastitis is one of the most frequent clinical diseases in dairy animals. Epithelial cells undergoing epithelial–mesenchymal transition (EMT) promote the process of mastitis. Oestrogen deficiency is disadvantaged of many tissue inflammation and regeneration, while exogenous oestrogen treatment can reverse these effects. G protein-coupled estrogen receptor 1 (GPER1) is a membrane estrogen receptor. However, the potential effects of oestrogen via GPER1 on EMT in goat mammary epithelial cells (GMECs) are still unclear. Here, this study discovered that the activation of GPER1 by oestrogen could inhibit the EMT in GMECs via NF-κB signalling pathway. The activation of GPER1 by oestrogen inhibited the EMT accompanied by upregulation of E-cadherin and downregulation of N-cadherin and vimentin. Meanwhile, mRNA expression of transcription factors including Snail1 and ZEB1 was decreased. Further, like to oestrogen, GPER1 agonist G1 repressed the EMT progression. Conversely, GPER1 antagonist G15 reversed all these features induced by oestrogen. What's more, GPER1 silencing with shRNA promoted GMECs undergoing EMT. Additionally, oestrogen increased the phosphorylation of Erk1/2, which then decreased the phosphorylation and nuclear translocation of NF-κB, inhibiting the NF-κB signalling pathway activity. Taken, GPER1 may act as a suppressor through the regulation of EMT to prevent the development of mastitis.</p>}},
author = {{Zhao, Ying and Yang, Zhenshan and Miao, Yuyang and Fan, Mingzhen and Zhao, Xiaoe and Wei, Qiang and Ma, Baohua}},
issn = {{0936-6768}},
keywords = {{epithelial-mesenchymal transition; G protein-coupled estrogen receptor 1; goat; mammary epithelial cells; oestrogen}},
language = {{eng}},
number = {{8}},
pages = {{1137--1144}},
publisher = {{Wiley-Blackwell}},
series = {{Reproduction in Domestic Animals}},
title = {{G protein-coupled estrogen receptor 1 inhibits the epithelial–mesenchymal transition of goat mammary epithelial cells via NF-κB signalling pathway}},
url = {{http://dx.doi.org/10.1111/rda.13957}},
doi = {{10.1111/rda.13957}},
volume = {{56}},
year = {{2021}},
}