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The proliferative effect of cortisol on bovine endometrial epithelial cells
BACKGROUND: Bovine endometrial epithelial cells (BEECs) undergo regular regeneration after calving. Elevated cortisol concentrations have been reported in postpartum cattle due to various stresses. However, the effects of the physiological level of cortisol on proliferation in BEECs have not been re...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6873581/ https://www.ncbi.nlm.nih.gov/pubmed/31757215 http://dx.doi.org/10.1186/s12958-019-0544-1 |
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author | Dong, Junsheng Li, Jun Li, Jianji Cui, Luying Meng, Xia Qu, Yang Wang, Heng |
author_facet | Dong, Junsheng Li, Jun Li, Jianji Cui, Luying Meng, Xia Qu, Yang Wang, Heng |
author_sort | Dong, Junsheng |
collection | PubMed |
description | BACKGROUND: Bovine endometrial epithelial cells (BEECs) undergo regular regeneration after calving. Elevated cortisol concentrations have been reported in postpartum cattle due to various stresses. However, the effects of the physiological level of cortisol on proliferation in BEECs have not been reported. The aim of this study was to investigate whether cortisol can influence the proliferation properties of BEECs and to clarify the possible underlying mechanism. METHODS: BEECs were treated with different concentrations of cortisol (5, 15 and 30 ng/mL). The mRNA expression of various growth factors was detected by quantitative reverse transcription-polymerase chain reaction (qPCR), progression of the cell cycle in BEECs was measured using flow cytometric analysis, and the activation of the Wnt/β-catenin and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways was detected with Western blot and immunofluorescence. RESULTS: Cortisol treatment resulted in upregulated mRNA levels of vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF); however, it had no influence on transforming growth factor-beta1 (TGF-β1). Cortisol (15 ng/mL) accelerated the cell cycle transition from the G0/G1 to the S phase. Cortisol upregulated the expression of β-catenin, c-Myc, and cyclinD1 and promoted the phosphorylation of PI3K and AKT. CONCLUSIONS: These results demonstrated that cortisol may promote proliferation in BEECs by increasing the expression of some growth factors and activating the Wnt/β-catenin and PI3K/AKT signaling pathways. |
format | Online Article Text |
id | pubmed-6873581 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-68735812019-11-25 The proliferative effect of cortisol on bovine endometrial epithelial cells Dong, Junsheng Li, Jun Li, Jianji Cui, Luying Meng, Xia Qu, Yang Wang, Heng Reprod Biol Endocrinol Research BACKGROUND: Bovine endometrial epithelial cells (BEECs) undergo regular regeneration after calving. Elevated cortisol concentrations have been reported in postpartum cattle due to various stresses. However, the effects of the physiological level of cortisol on proliferation in BEECs have not been reported. The aim of this study was to investigate whether cortisol can influence the proliferation properties of BEECs and to clarify the possible underlying mechanism. METHODS: BEECs were treated with different concentrations of cortisol (5, 15 and 30 ng/mL). The mRNA expression of various growth factors was detected by quantitative reverse transcription-polymerase chain reaction (qPCR), progression of the cell cycle in BEECs was measured using flow cytometric analysis, and the activation of the Wnt/β-catenin and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways was detected with Western blot and immunofluorescence. RESULTS: Cortisol treatment resulted in upregulated mRNA levels of vascular endothelial growth factor (VEGF) and connective tissue growth factor (CTGF); however, it had no influence on transforming growth factor-beta1 (TGF-β1). Cortisol (15 ng/mL) accelerated the cell cycle transition from the G0/G1 to the S phase. Cortisol upregulated the expression of β-catenin, c-Myc, and cyclinD1 and promoted the phosphorylation of PI3K and AKT. CONCLUSIONS: These results demonstrated that cortisol may promote proliferation in BEECs by increasing the expression of some growth factors and activating the Wnt/β-catenin and PI3K/AKT signaling pathways. BioMed Central 2019-11-22 /pmc/articles/PMC6873581/ /pubmed/31757215 http://dx.doi.org/10.1186/s12958-019-0544-1 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 Dong, Junsheng Li, Jun Li, Jianji Cui, Luying Meng, Xia Qu, Yang Wang, Heng The proliferative effect of cortisol on bovine endometrial epithelial cells |
title | The proliferative effect of cortisol on bovine endometrial epithelial cells |
title_full | The proliferative effect of cortisol on bovine endometrial epithelial cells |
title_fullStr | The proliferative effect of cortisol on bovine endometrial epithelial cells |
title_full_unstemmed | The proliferative effect of cortisol on bovine endometrial epithelial cells |
title_short | The proliferative effect of cortisol on bovine endometrial epithelial cells |
title_sort | proliferative effect of cortisol on bovine endometrial epithelial cells |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6873581/ https://www.ncbi.nlm.nih.gov/pubmed/31757215 http://dx.doi.org/10.1186/s12958-019-0544-1 |
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