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Cortisol Excess-Mediated Mitochondrial Damage Induced Hippocampal Neuronal Apoptosis in Mice Following Cold Exposure

Cold stress can induce neuronal apoptosis in the hippocampus, but the internal mechanism involving neuronal loss induced by cold stress is not clear. In vivo, male and female C57BL/6 mice were exposed to 4 °C, 3 h per day for 1 week. In vitro, HT22 cells were treated with different concentrations of...

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Autores principales: Xu, Bin, Lang, Li-min, Li, Shi-Ze, Guo, Jing-Ru, Wang, Jian-Fa, Wang, Di, Zhang, Li-Ping, Yang, Huan-Min, Lian, Shuai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627841/
https://www.ncbi.nlm.nih.gov/pubmed/31216749
http://dx.doi.org/10.3390/cells8060612
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author Xu, Bin
Lang, Li-min
Li, Shi-Ze
Guo, Jing-Ru
Wang, Jian-Fa
Wang, Di
Zhang, Li-Ping
Yang, Huan-Min
Lian, Shuai
author_facet Xu, Bin
Lang, Li-min
Li, Shi-Ze
Guo, Jing-Ru
Wang, Jian-Fa
Wang, Di
Zhang, Li-Ping
Yang, Huan-Min
Lian, Shuai
author_sort Xu, Bin
collection PubMed
description Cold stress can induce neuronal apoptosis in the hippocampus, but the internal mechanism involving neuronal loss induced by cold stress is not clear. In vivo, male and female C57BL/6 mice were exposed to 4 °C, 3 h per day for 1 week. In vitro, HT22 cells were treated with different concentrations of cortisol (CORT) for 3 h. In vivo, CORT levels in the hippocampus were measured using ELISA, western blotting, and immunohistochemistry to assess the neuronal population and oxidation of the hippocampus. In vitro, western blotting, immunofluorescence, flow cytometry, transmission electron microscopy, and other methods were used to characterize the mechanism of mitochondrial damage induced by CORT. The phenomena of excessive CORT-mediated oxidation stress and neuronal apoptosis were shown in mouse hippocampus tissue following cold exposure, involving mitochondrial oxidative stress and endogenous apoptotic pathway activation. These processes were mediated by acetylation of lysine 9 of histone 3, resulting in upregulation involving Adenosine 5‘-monophosphate (AMP)-activated protein kinase (APMK) phosphorylation and translocation of Nrf2 to the nucleus. In addition, oxidation in male mice was more severe. These findings provide a new understanding of the underlying mechanisms of the cold stress response and explain the apoptosis process induced by CORT, which may influence the selection of animal models in future stress-related studies.
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spelling pubmed-66278412019-07-23 Cortisol Excess-Mediated Mitochondrial Damage Induced Hippocampal Neuronal Apoptosis in Mice Following Cold Exposure Xu, Bin Lang, Li-min Li, Shi-Ze Guo, Jing-Ru Wang, Jian-Fa Wang, Di Zhang, Li-Ping Yang, Huan-Min Lian, Shuai Cells Article Cold stress can induce neuronal apoptosis in the hippocampus, but the internal mechanism involving neuronal loss induced by cold stress is not clear. In vivo, male and female C57BL/6 mice were exposed to 4 °C, 3 h per day for 1 week. In vitro, HT22 cells were treated with different concentrations of cortisol (CORT) for 3 h. In vivo, CORT levels in the hippocampus were measured using ELISA, western blotting, and immunohistochemistry to assess the neuronal population and oxidation of the hippocampus. In vitro, western blotting, immunofluorescence, flow cytometry, transmission electron microscopy, and other methods were used to characterize the mechanism of mitochondrial damage induced by CORT. The phenomena of excessive CORT-mediated oxidation stress and neuronal apoptosis were shown in mouse hippocampus tissue following cold exposure, involving mitochondrial oxidative stress and endogenous apoptotic pathway activation. These processes were mediated by acetylation of lysine 9 of histone 3, resulting in upregulation involving Adenosine 5‘-monophosphate (AMP)-activated protein kinase (APMK) phosphorylation and translocation of Nrf2 to the nucleus. In addition, oxidation in male mice was more severe. These findings provide a new understanding of the underlying mechanisms of the cold stress response and explain the apoptosis process induced by CORT, which may influence the selection of animal models in future stress-related studies. MDPI 2019-06-18 /pmc/articles/PMC6627841/ /pubmed/31216749 http://dx.doi.org/10.3390/cells8060612 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Xu, Bin
Lang, Li-min
Li, Shi-Ze
Guo, Jing-Ru
Wang, Jian-Fa
Wang, Di
Zhang, Li-Ping
Yang, Huan-Min
Lian, Shuai
Cortisol Excess-Mediated Mitochondrial Damage Induced Hippocampal Neuronal Apoptosis in Mice Following Cold Exposure
title Cortisol Excess-Mediated Mitochondrial Damage Induced Hippocampal Neuronal Apoptosis in Mice Following Cold Exposure
title_full Cortisol Excess-Mediated Mitochondrial Damage Induced Hippocampal Neuronal Apoptosis in Mice Following Cold Exposure
title_fullStr Cortisol Excess-Mediated Mitochondrial Damage Induced Hippocampal Neuronal Apoptosis in Mice Following Cold Exposure
title_full_unstemmed Cortisol Excess-Mediated Mitochondrial Damage Induced Hippocampal Neuronal Apoptosis in Mice Following Cold Exposure
title_short Cortisol Excess-Mediated Mitochondrial Damage Induced Hippocampal Neuronal Apoptosis in Mice Following Cold Exposure
title_sort cortisol excess-mediated mitochondrial damage induced hippocampal neuronal apoptosis in mice following cold exposure
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627841/
https://www.ncbi.nlm.nih.gov/pubmed/31216749
http://dx.doi.org/10.3390/cells8060612
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