HMGB1 mediates depressive behavior induced by chronic stress through activating the kynurenine pathway

Wang, Bo; Lian, Yong‐Jie; Su, Wen‐Jun; Wei, Peng; Dong, Xin; Liu, Linlin; Gong, Hongyun; Zou, Ting; Jiang, Chun‐Lei; Wang, Yunxia

doi:10.1016/j.bbi.2017.11.017

Cited by 87 publications

(56 citation statements)

References 72 publications

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“…In human literature, subjects with major depressive disorder have been found to have a significant increase in circulating T H 17 cells and a significant decrease in T reg cells (and thus an increased ratio) when measured by flow cytometry; increased levels of RORγT; and higher levels of circulating IL-17 when compared to healthy controls (Chen et al, 2011); and increases in both IL-17 and the stimulating cytokine TGF-β compared to age-matched controls (Davami et al, 2016). Mouse models have indicated that elevated HMGB1 is associated with increased depressivelike symptoms as well (Franklin et al, 2018;Wang et al, 2018;Wu et al, 2015).…”

Section: Depressionmentioning

confidence: 99%

The role of Th17 cells in the pathophysiology of pregnancy and perinatal mood and anxiety disorders

Osborne

Brar

Klein

2019

Brain, Behavior, and Immunity

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T cells play a key role in adaptive immune responses, and shifts among T cell classes occur in normal pregnancy. There is evidence for the role of T H 17 cells and dysregulation of the T H 17:T reg cell balance in morbidities and autoimmune diseases during pregnancy. Because T H 17 responses may play a role in depression and anxiety outside of pregnancy, we hypothesize that T H 17 responses and the balance of T H 17:T reg activity may also contribute to the development of depression and anxiety during pregnancy. To explore this hypothesis, this review has three main aims: 1) to evaluate systematically the role of T H 17 cells and cytokines during pregnancy; 2) to compare changes in the ratio of T H 17:T reg cells during pregnancy morbidities with the changes that occur in depression and anxiety outside of pregnancy; and 3) to provide a basis for further research on T H 17 cells in perinatal mood and anxiety disorders, with an eye toward the development of novel therapeutics. We also review the limited literature concerning perinatal mood and anxiety disorders, and hypothesize about the potential role of T H 17 cells in these illnesses. Understanding the pathophysiology of perinatal mood and anxiety disorders will aid development of novel therapeutics that address immunological mechanisms, in addition to the serotonin system, which are targetable molecules in treating depression and anxiety during pregnancy.

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Section: Depressionmentioning

confidence: 99%

The role of Th17 cells in the pathophysiology of pregnancy and perinatal mood and anxiety disorders

Osborne

Brar

Klein

2019

Brain, Behavior, and Immunity

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“…The spared nerve injury (SNI) model also confirmed that stressed mice were characterized by increased mRNA and Kmo protein expression mostly in the hippocampal neurons [ 48 ]. On the other hand, Wang et al (2018) observed no differences in Kmo activity between control and chronic unpredictable mild stress groups [ 49 ]. In the case of KatII, CMS caused a downregulation of mRNA expression in the cortex [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

The Impact of Chronic Mild Stress and Agomelatine Treatment on the Expression Level and Methylation Status of Genes Involved in Tryptophan Catabolic Pathway in PBMCs and Brain Structures

Wigner

Synowiec

Jóźwiak

et al. 2020

Genes

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Depression is the serious mental disorder. Previous studies suggest that the development mechanism of depression may be associated with disorders of the tryptophan catabolic pathway (TRYCAT). Thus, this study investigates the effect of agomelatine treatment on the expression and methylation status of genes involved in TRYCAT in the brain and blood of rats exposed to a chronic mild stress (CMS). Separate groups of rats were exposed to CMS for two or seven weeks; the second group received vehicle or agomelatine for five weeks. After completion of both stress conditions and treatment, the expression levels of messenger RNA (mRNA) and protein, as well as the methylation status of promoters, were measured in peripheral blood mononuclear cells (PBMCs) and in brain structures with the use of TaqMan Gene Expression Assay, Western blot, and methylation-sensitive high-resolution melting techniques. In PBMCs, Kmo mRNA expression increased in the group after CMS, while this effect was normalized by agomelatine therapy. In brain, KatI and KatII expression changed following CMS exposure. Moreover, CMS decreased the methylation status of the second Tdo2 promoter in the amygdala. Protein expression of Tph1, Tph2, Ido1, and KatII changed in the group after CMS and agomelatine administration, most prominently in the basal ganglia, cerebral cortex, hippocampus, and amygdala. The results indicate that CMS and agomelatine affect the mRNA and protein expression, as well as the methylation of promoters of genes involved in the tryptophan catabolic pathway.

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“…For spatial learning and memory assessment we used a 122-cm diameter Barnes maze elevated 140 cm above the floor and that contains 20 holes, each 5 cm in diameter, located evenly on the periphery of the surface. One of these holes was connected to a dark chamber called target box, which allowed the mouse to escape from an aversive bright light (200 W) ( Akman et al, 2015 ; Wang et al, 2017 ). Animals were firstly placed in a black cylinder at the center of the maze for 15 s. Subsequently, the cylinder was removed and the mouse explored the maze until it found and entered the target box.…”

Section: Methodsmentioning

confidence: 99%

Inhibiting RIP1 Improves Chronic Stress-Induced Cognitive Impairments in D-Galactose-Induced Aging Mice

Wang

et al. 2018

Front. Behav. Neurosci.

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Mounting evidence shows that chronic stress can affect both the structure and function of the brain resulting in decreased synaptic plasticity and cognitive dysfunction. Although several studies have indicated that aged brains are more vulnerable to chronic stress, it remains unknown how to prevent stress-induced memory deficits in aged animals. Neuroinflammation plays an important role in the pathogenesis of chronic stress-related brain dysfunction. Receptor-interacting protein 1 (RIP1) is a key molecule that can modulate inflammation, apoptosis, and necroptosis. Here, we investigated whether inhibiting RIP1 using necrostatin-1 during chronic stress could improve chronic stress-related brain dysfunction in D-galactose-induced aging mice. The stressed mice underwent restraint stress for 14 days. Necrostatin-1 (6.25 mg/kg) or vehicle was administered intraperitoneally once every 3 days during the stress period. Locomotor activity was tested using the open field test and cognitive function was assessed using the novel object recognition and Barnes maze tests. The hippocampus was collected to assess neuroinflammation (Iba1, IL-1α, IL-1β, TNF-α, and C1q), necroptosis [RIP1, RIP3, mixed lineage kinase domain-like (MLKL), and NF-κB], neuroplasticity (doublecortin, NR1, NR2A, NR2B, GluA1, and GluA2), and the expression of glucocorticoid and mineralocorticoid receptors. Blood samples were collected to quantify the levels of corticosterone. We found that chronic stress induced obvious memory impairment and neuroinflammation, decreased neurogenesis and GluA2 expression, and increased the expression of RIP1 and NF-κB. Inhibiting RIP1 by necrostatin-1 during chronic stress rescued the memory impairment and alleviated the pathological changes induced by stress. These suggest that inhibiting RIP1 using necrostatin-1 improves chronic stress-related brain dysfunction in D-galactose-induced aging mice. The potential mechanisms include limitation of neuroinflammation and the rescue of neurogenesis and GluA2 expression.

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HMGB1 mediates depressive behavior induced by chronic stress through activating the kynurenine pathway

Cited by 87 publications

References 72 publications

The role of Th17 cells in the pathophysiology of pregnancy and perinatal mood and anxiety disorders

The role of Th17 cells in the pathophysiology of pregnancy and perinatal mood and anxiety disorders

The Impact of Chronic Mild Stress and Agomelatine Treatment on the Expression Level and Methylation Status of Genes Involved in Tryptophan Catabolic Pathway in PBMCs and Brain Structures

Inhibiting RIP1 Improves Chronic Stress-Induced Cognitive Impairments in D-Galactose-Induced Aging Mice

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