Cargando…
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...
Autores principales: | , , , , , , , , |
---|---|
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 |
_version_ | 1783434827507171328 |
---|---|
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. |
format | Online Article Text |
id | pubmed-6627841 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT xubin cortisolexcessmediatedmitochondrialdamageinducedhippocampalneuronalapoptosisinmicefollowingcoldexposure AT langlimin cortisolexcessmediatedmitochondrialdamageinducedhippocampalneuronalapoptosisinmicefollowingcoldexposure AT lishize cortisolexcessmediatedmitochondrialdamageinducedhippocampalneuronalapoptosisinmicefollowingcoldexposure AT guojingru cortisolexcessmediatedmitochondrialdamageinducedhippocampalneuronalapoptosisinmicefollowingcoldexposure AT wangjianfa cortisolexcessmediatedmitochondrialdamageinducedhippocampalneuronalapoptosisinmicefollowingcoldexposure AT wangdi cortisolexcessmediatedmitochondrialdamageinducedhippocampalneuronalapoptosisinmicefollowingcoldexposure AT zhangliping cortisolexcessmediatedmitochondrialdamageinducedhippocampalneuronalapoptosisinmicefollowingcoldexposure AT yanghuanmin cortisolexcessmediatedmitochondrialdamageinducedhippocampalneuronalapoptosisinmicefollowingcoldexposure AT lianshuai cortisolexcessmediatedmitochondrialdamageinducedhippocampalneuronalapoptosisinmicefollowingcoldexposure |