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Low Concentrations of Corticosterone Exert Stimulatory Effects on Macrophage Function in a Manner Dependent on Glucocorticoid Receptors
Endogenous glucocorticoids (GCs) have both stimulatory and suppressive effects on immune cells depending on the concentration. However, the mechanisms underlying the stimulatory effects of GCs remain elusive. Rat peritoneal macrophages were treated with different concentrations of corticosterone (0,...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3806411/ https://www.ncbi.nlm.nih.gov/pubmed/24194757 http://dx.doi.org/10.1155/2013/405127 |
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author | Zhong, He-Jiang Wang, Hai-Yan Yang, Ce Zhou, Jian-Yun Jiang, Jian-Xin |
author_facet | Zhong, He-Jiang Wang, Hai-Yan Yang, Ce Zhou, Jian-Yun Jiang, Jian-Xin |
author_sort | Zhong, He-Jiang |
collection | PubMed |
description | Endogenous glucocorticoids (GCs) have both stimulatory and suppressive effects on immune cells depending on the concentration. However, the mechanisms underlying the stimulatory effects of GCs remain elusive. Rat peritoneal macrophages were treated with different concentrations of corticosterone (0, 30 nM, 150 nM, and 3 μM). To inhibit the glucocorticoid receptor (GR) activity, macrophages were preincubated with the GR antagonist RU486 (mifepristone, 10 μM) for 30 min before treatment with corticosterone (150 nM). In the absence of immune stimuli, the chemotactic and phagocytic activities of macrophages were markedly enhanced by low concentrations of corticosterone (30 and 150 nM) when compared with vehicle-treated controls. However, these effects were not observed at a high concentration of corticosterone (3 μM). Furthermore, blocking GR activity inhibited 150 nM corticosterone-enhanced chemotaxis and phagocytosis of macrophages. Meanwhile, after treatment with corticosterone (150 nM) for 1 h and 3 h, GR protein expression increased to 1.4- and 2.2-fold, respectively, compared to untreated macrophages. These effects were inhibited by RU486. However, mineralocorticoid receptor (MR) protein expression was not influenced by 150 nM corticosterone. These results demonstrate that low concentrations of corticosterone exert stimulatory effects on macrophage function in the absence of immune stimuli, and GR is at least partially responsible for these effects. |
format | Online Article Text |
id | pubmed-3806411 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-38064112013-11-05 Low Concentrations of Corticosterone Exert Stimulatory Effects on Macrophage Function in a Manner Dependent on Glucocorticoid Receptors Zhong, He-Jiang Wang, Hai-Yan Yang, Ce Zhou, Jian-Yun Jiang, Jian-Xin Int J Endocrinol Research Article Endogenous glucocorticoids (GCs) have both stimulatory and suppressive effects on immune cells depending on the concentration. However, the mechanisms underlying the stimulatory effects of GCs remain elusive. Rat peritoneal macrophages were treated with different concentrations of corticosterone (0, 30 nM, 150 nM, and 3 μM). To inhibit the glucocorticoid receptor (GR) activity, macrophages were preincubated with the GR antagonist RU486 (mifepristone, 10 μM) for 30 min before treatment with corticosterone (150 nM). In the absence of immune stimuli, the chemotactic and phagocytic activities of macrophages were markedly enhanced by low concentrations of corticosterone (30 and 150 nM) when compared with vehicle-treated controls. However, these effects were not observed at a high concentration of corticosterone (3 μM). Furthermore, blocking GR activity inhibited 150 nM corticosterone-enhanced chemotaxis and phagocytosis of macrophages. Meanwhile, after treatment with corticosterone (150 nM) for 1 h and 3 h, GR protein expression increased to 1.4- and 2.2-fold, respectively, compared to untreated macrophages. These effects were inhibited by RU486. However, mineralocorticoid receptor (MR) protein expression was not influenced by 150 nM corticosterone. These results demonstrate that low concentrations of corticosterone exert stimulatory effects on macrophage function in the absence of immune stimuli, and GR is at least partially responsible for these effects. Hindawi Publishing Corporation 2013 2013-10-01 /pmc/articles/PMC3806411/ /pubmed/24194757 http://dx.doi.org/10.1155/2013/405127 Text en Copyright © 2013 He-Jiang Zhong et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Zhong, He-Jiang Wang, Hai-Yan Yang, Ce Zhou, Jian-Yun Jiang, Jian-Xin Low Concentrations of Corticosterone Exert Stimulatory Effects on Macrophage Function in a Manner Dependent on Glucocorticoid Receptors |
title | Low Concentrations of Corticosterone Exert Stimulatory Effects on Macrophage Function in a Manner Dependent on Glucocorticoid Receptors |
title_full | Low Concentrations of Corticosterone Exert Stimulatory Effects on Macrophage Function in a Manner Dependent on Glucocorticoid Receptors |
title_fullStr | Low Concentrations of Corticosterone Exert Stimulatory Effects on Macrophage Function in a Manner Dependent on Glucocorticoid Receptors |
title_full_unstemmed | Low Concentrations of Corticosterone Exert Stimulatory Effects on Macrophage Function in a Manner Dependent on Glucocorticoid Receptors |
title_short | Low Concentrations of Corticosterone Exert Stimulatory Effects on Macrophage Function in a Manner Dependent on Glucocorticoid Receptors |
title_sort | low concentrations of corticosterone exert stimulatory effects on macrophage function in a manner dependent on glucocorticoid receptors |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3806411/ https://www.ncbi.nlm.nih.gov/pubmed/24194757 http://dx.doi.org/10.1155/2013/405127 |
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