HMGB1-mediated differential response on hippocampal neurotransmitter disorder and neuroinflammation in adolescent male and female mice following cold exposure

Xu, Bin; Zang, Shucheng; Li, Shize; Guo, Jiang; Wang, Jianfa; Wang, Di; Zhang, Liping; Yang, Huanmin; Lian, Shuai

doi:10.1016/j.bbi.2018.11.313

Cited by 34 publications

(35 citation statements)

References 46 publications

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“…Stage of the estrous cycle is critical when examining the effects of acute stress exposure on brain cytokine induction, because estrogen has anti-inflammatory effects on the induction of IL-1 β after foot shock [52]. In addition, IL-6 and TNF- α production is reduced in the hippocampus of female mice after repeated cold stress, compared with male mice [53]. The largest sex difference appears to be on the effects of chronic stress on microglia themselves.…”

Section: Discussionmentioning

confidence: 99%

Neuroendocrine Regulation of Brain Cytokines After Psychological Stress

Johnson

Barnard

Kulp

et al. 2019

Journal of the Endocrine Society

102

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There is growing evidence that stress-induced brain cytokines are important in the etiology of depression and anxiety. Here, we review how the neuroendocrine responses to psychological stressors affect the immediate and long-term regulation of inflammatory cytokines within the brain and highlight how the regulation changes across time with repeated stress exposure. In doing so, we report on the percentage of studies in the literature that observed increases in either IL-1 β , TNF- α , or IL-6 within the hypothalamus, hippocampus, or prefrontal cortex after either acute or chronic stress exposure. The key takeaway is that catecholamines and glucocorticoids play critical roles in the regulation of brain cytokines after psychological stress exposure. Central catecholamines stimulate the release of IL-1 β from microglia, which is a key factor in the further activation of microglia and recruitment of monocytes into the brain. Meanwhile, the acute elevation of glucocorticoids inhibits the production of brain cytokines via two mechanisms: the suppression of noradrenergic locus coeruleus neurons and inhibition of the NF κ B signaling pathway. However, glucocorticoids and peripheral catecholamines facilitate inflammatory responses to future stimuli by stimulating monocytes to leave the bone marrow, downregulating inhibitory receptors on microglia, and priming inflammatory responses mediated by peripheral monocytes or macrophages. The activation of microglia and the elevation of peripheral glucocorticoid and catecholamine levels are both necessary during times of stress exposure for the development of psychopathologies.

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Section: Discussionmentioning

confidence: 99%

Neuroendocrine Regulation of Brain Cytokines After Psychological Stress

Johnson

Barnard

Kulp

et al. 2019

Journal of the Endocrine Society

102

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“…Bcl2 is widely known as an important anti-apoptotic molecule in tumour and normal cells (Cui & Placzek, 2018;Maes, Schlamp, & Nickells, 2017). Bcl2 can exert its anti-apoptotic effect by inhibiting the release of Cyto C by changing mitochondrial permeability and competing with the pro-apoptotic molecule (Bax) to form a heterodimer (Xu et al, 2019). These results shown that miR-383-5p may promote the oxidative damage of rat hepatocytes induced by H 2 O 2 by targeting inhibition of Bcl2 protein translation, and the abnormal down-regulation of miR-383-5p in rat liver after cold stimulation is likely to be the response of an organism to protect the liver from hypothermia ( Figure 6).…”

Section: Discussionmentioning

confidence: 99%

Down‐regulation of miR‐383‐5p suppresses apoptosis in oxidative stress rat hepatocytes by targeting Bcl2

Zang

Lang

et al. 2020

Animal Physiology Nutrition

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When humans or animals are exposed to low temperatures for a long time, the damage caused by low temperatures will be resisted through a series of biological reactions; the non-specific reaction is referred to as the cold stress response (Klepikova, Kulakovskiy, Kasianov, Logacheva, & Penin, 2019). Living at low temperatures has effects on cell development, production performance, metabolism function and bodily functions, thus affecting the growth and development of an organism. Therefore, it is very important to study the mechanism underlying cold stress. Indeed, the mechanism of cold stress is quite complex and almost all organs and tissues are involved

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“…The in vivo results supported our hypothesis. First, the chronic cold stress model was developed based on our previous report [10]. Next, the CORT level of the mouse hippocampus after cold exposure was measured, showing that the CORT level of the hippocampus significantly increased in the CEM and CEF groups, and the specific expression of GR receptors was also increased in the same groups.…”

Section: Discussionmentioning

confidence: 99%

“…Cold stress syndrome induced by cold exposure disturbs energy metabolism and immunological functions [7], resulting in endogenous or secondary diseases [8,9]. In our previous study, cold stress in mice induced by cold exposure was built systematically and the process of neuronal loss in the CA1 and CA3 regions of mice following cold exposure was reported [10], but the internal mechanism of neuronal loss and cold stress is still not clear.…”

Section: Introductionmentioning

confidence: 99%

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

Lang

et al. 2019

Cells

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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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HMGB1-mediated differential response on hippocampal neurotransmitter disorder and neuroinflammation in adolescent male and female mice following cold exposure

Cited by 34 publications

References 46 publications

Neuroendocrine Regulation of Brain Cytokines After Psychological Stress

Neuroendocrine Regulation of Brain Cytokines After Psychological Stress

Down‐regulation of miR‐383‐5p suppresses apoptosis in oxidative stress rat hepatocytes by targeting Bcl2

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

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