Corticosterone Induces HMGB1 Release in Primary Cultured Rat Cortical Astrocytes: Involvement of Pannexin-1 and P2X7 Receptor-Dependent Mechanisms

Hisaoka-Nakashima, Kazue; Azuma, Honami; Ishikawa, Fumina; Nakamura, Yoki; Wang, Dengli; Liu, Keyue; Wake, Hidenori; Nishibori, Masahiro; Nakata, Yoshihiro; Morioka, Norimitsu

doi:10.3390/cells9051068

Cited by 22 publications

(11 citation statements)

References 66 publications

(49 reference statements)

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“…HMGB1 has been implicated in the stress-induced sensitization of innate immune cells and subsequent neuroinflammation ( Zhang et al, 2019 ). Also, it has been suggested that, under stress, GC may induce HMGB1 release ( Frank et al, 2015 ; Hisaoka-Nakashima et al, 2020 ).…”

Section: Immune System and Inflammationmentioning

confidence: 99%

Stress System Activation in Children and Adolescents With Autism Spectrum Disorder

et al. 2022

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The mission of the human stress system is the maintenance of homeostasis in the presence of real or perceived, acute or chronic stressors. The hypothalamic–pituitary–adrenal (HPA) axis and the autonomic nervous system (ANS) are the stress system-related neuroendocrine pathways. There is abundant evidence that children and adolescents with autism spectrum disorder (ASD) may exhibit atypical function within the HPA axis and the ANS both at the resting state and during the presence of social and/or non-social stressors. The aim of this review is to provide an up-to-date summary of the findings regarding stress system alterations in children and adolescents with ASD. We focus on the variations of stress hormones circadian rhythms, specifically cortisol and alpha-amylase (i.e., a surrogate index of epinephrine/norepinephrine secretion), and on the alterations of stress system responsivity to different stressors. Also, we present imaging and immunological findings that have been associated with stress system dysregulation in children and adolescents with ASD. Finally, we review the pivotal role of HPA axis-ANS coordination, the developmental trajectory of the stress system in ASD, and the possible role of early life stress in the dysregulation of the stress system demonstrated in children and adolescents with ASD. This synthesis will hopefully provide researchers with a foundation for an integrated approach to future research into stress system variations in children and adolescents with ASD.

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Section: Immune System and Inflammationmentioning

confidence: 99%

Stress System Activation in Children and Adolescents With Autism Spectrum Disorder

et al. 2022

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“…After drug treatment, media were collected and concentrated with trichloroacetic acid (catalog # 203‐04952; FUJIFILM Wako Pure Chemical Corporation, ). Concentrated media sample or cells were lysed with radio immunoprecipitation assay buffer (RIPA buffer) with inhibitors (100 mM Tris–HCl, pH 7.4, 150 mM NaCl, 1 mM EDTA, 1% Triton X‐100, 1% sodium deoxycholate, 0.1% sodium dodecyl sulfate (SDS), 20 µg/ml aprotinin, 20 µg/ml leupeptin, 1 mM phenylmethylsulfonyl fluoride, and phosphatase inhibitor cocktail (Nacalai Tesque, )) as described previously (Hisaoka‐Nakashima et al., 2020). Equal amounts of protein were separated by 12% SDS–polyacrylamide gel electrophoresis and blotted onto PVDF membranes.…”

Section: Methodsmentioning

confidence: 99%

“…Immunocytochemistry of primary cultured rat cortical astrocytes was performed as described previously (Hisaoka‐Nakashima et al., 2020). Astrocytes were treated with LPA for 3 hr, and after washing, cells were fixed in 4% paraformaldehyde in PBS for 30 min.…”

Section: Methodsmentioning

confidence: 99%

Lysophosphatidic acid induces thrombospondin‐1 production in primary cultured rat cortical astrocytes

Hisaoka-Nakashima

Yokoe

Watanabe

et al. 2020

Journal of Neurochemistry

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Lysophosphatidic acid (LPA), a brain membrane‐derived lipid mediator, plays important roles including neural development, function, and behavior. In the present study, the effects of LPA on astrocyte‐derived synaptogenesis factor thrombospondins (TSPs) production were examined by real‐time PCR and western blotting, and the mechanism underlying this event was examined by pharmacological approaches in primary cultured rat cortical astrocytes. Treatment of astrocytes with LPA increased TSP‐1 mRNA, and TSP‐2 mRNA, but not TSP‐4 mRNA expression. TSP‐1 protein expression and release were also increased by LPA. LPA‐induced TSP‐1 production were inhibited by AM966 a LPA1 receptor antagonist, and Ki16425, LPA1/3 receptors antagonist, but not by H2L5146303, LPA2 receptor antagonist. Pertussis toxin, Gi/o inhibitor, but not YM‐254890, Gq inhibitor, and NF499, Gs inhibitor, inhibited LPA‐induced TSP‐1 production, indicating that LPA increases TSP‐1 production through Gi/o‐coupled LPA1 and LPA3 receptors. LPA treatment increased phosphorylation of extracellular signal‐regulated kinase (ERK), p38 mitogen‐activated protein kinase (MAPK), and c‐Jun N‐terminal kinase (JNK). LPA‐induced TSP‐1 mRNA expression was inhibited by U0126, MAPK/ERK kinase (MEK) inhibitor, but not SB202190, p38 MAPK inhibitor, or SP600125, JNK inhibitor. However, LPA‐induced TSP‐1 protein expression was diminished with inhibition of all three MAPKs, indicating that these signaling molecules are involved in TSP‐1 protein production. Treatment with antidepressants, which bind to astrocytic LPA1 receptors, increased TSP‐1 mRNA and protein production. The current findings show that LPA/LPA1/3 receptors signaling increases TSP‐1 production in astrocytes, which could be important in the pathogenesis of affective disorders and could potentially be a target for the treatment of affective disorders.

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“…Moreover, chronic activation causes astrocytes to produce high levels of chemokines (Gimsa et al, 2013). Furthermore, hippocampal astrocytes mediate the depressive behavior induced by chronic stress (Hisaoka-Nakashima et al, 2020;Du Preez et al, 2021). Taken together, these findings indicate that dynamic changes in glia and their interactions contribute to the inflammatory processes involved in depression.…”

Section: Introductionmentioning

confidence: 92%

Microglia Loss and Astrocyte Activation Cause Dynamic Changes in Hippocampal [18F]DPA-714 Uptake in Mouse Models of Depression

Guo

Qiu

Wang

et al. 2022

Front. Cell. Neurosci.

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Major depression is a serious and chronic mental illness. However, its etiology is poorly understood. Although glial cells have been increasingly implicated in the pathogenesis of depression, the specific role of microglia and astrocytes in stress-induced depression remains unclear. Translocator protein (TSPO) has long been considered a marker of neuroinflammation and microglial activation. However, this protein is also present on astrocytes. Thus, it is necessary to explore the relationships between TSPO, microglia, and astrocytes in the context of depression. In this study, C57BL/6J male mice were subjected to chronic unpredictable stress (CUS) for 5 weeks. Subsequently, sucrose preference and tail suspension tests (TSTs) were performed to assess anhedonia and despair in these mice. [18F]DPA-714 positron emission tomography (PET) was adopted to dynamically assess the changes in glial cells before and 2, 4, or 5 weeks after CUS exposure. The numbers of TSPO+ cells, ionized calcium-binding adaptor molecule (Iba)-1+ microglial cells, TSPO+/Iba-1+ cells, glial fibrillary acidic protein (GFAP)+ astrocytes, TSPO+/GFAP+ cells, and TUNEL-stained microglia were quantified using immunofluorescence staining. Real-time PCR was used to evaluate interleukin (IL)-1β, IL-4, and IL-18 expression in the hippocampus. We observed that hippocampal [18F]DPA-714 uptake significantly increased after 2 weeks of CUS. However, the signal significantly decreased after 5 weeks of CUS. CUS significantly reduced the number of Iba-1+, TSPO+, and TSPO+/Iba-1+ cells in the hippocampus, especially in the CA1 and dentate gyrus (DG) subregions. However, this intervention increased the number of GFAP+ astrocytes in the CA2/CA3 subregions of the hippocampus. In addition, microglial apoptosis in the early stage of CUS appeared to be involved in microglia loss. Further, the expression of pro-inflammatory cytokines (IL-1β and IL-18) was significantly decreased after CUS. In contrast, the expression of the anti-inflammatory cytokine IL-4 was significantly increased after 2 weeks of CUS. These results suggested that the CUS-induced dynamic changes in hippocampal [18F]DPA-714 uptake and several cytokines may be due to combined microglial and astrocyte action. These findings provide a theoretical reference for the future clinical applications of TSPO PET.

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Corticosterone Induces HMGB1 Release in Primary Cultured Rat Cortical Astrocytes: Involvement of Pannexin-1 and P2X7 Receptor-Dependent Mechanisms

Cited by 22 publications

References 66 publications

Stress System Activation in Children and Adolescents With Autism Spectrum Disorder

Stress System Activation in Children and Adolescents With Autism Spectrum Disorder

Lysophosphatidic acid induces thrombospondin‐1 production in primary cultured rat cortical astrocytes

Microglia Loss and Astrocyte Activation Cause Dynamic Changes in Hippocampal [18F]DPA-714 Uptake in Mouse Models of Depression

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