The cystathionine β-synthase/hydrogen sulfide pathway contributes to microglia-mediated neuroinflammation following cerebral ischemia

Zhang, Minjie; Wu, Xiaowei; Xu, Yingxiu; He, Meijun; Yang, Jiaying; Li, Jie; Li, Yuyao; Ao, Gui-Zhen; Cheng, Jian; Jia, Jia

doi:10.1016/j.bbi.2017.07.156

Cited by 71 publications

(44 citation statements)

References 51 publications

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“…One of the pathophysiological effects in trout after UEI is assumed to be microglial polarization with appearance of clusters of activated microglia with a pro-inflammatory phenotype (Figure 4). Similar effects were also identified in a cell culture with exogenous administration of sodium hydrosulfide [36]. Thus, an…”

Section: Optic Tectumsupporting

confidence: 69%

Hydrogen Sulfide as a Factor of Neuroprotection during the Constitutive and Reparative Neurogenesis in Fish Brain

Пущина¹,

Вараксин²,

Обухов³

2020

Neuroprotection - New Approaches and Prospects

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The H 2 S-producing systems were studied in trout telencephalon, tectum, and cerebellum at 1 week after eye injury. The results of ELISA analysis have shown a 1.7-fold increase in the CBS expression at 1 week post-injury, as compared to the intact trout. In the ventricular and subventricular regions of trout telencephalon, CBS+ cells, as well as neuroepithelial and glial types, were detected. As a result of injury, the number of CBS+ neuroepithelial cells in the pallial and subpallial periventricular regions of the telencephalon increases. In the tectum, a traumatic damage leads to an increase in the CBS expression in radial glia with a simultaneous decrease in the number of CBS immunopositive neuroepithelial cells detected in intact animals. In the cerebellum, we revealed neuroglial interrelations, in which H 2 S is probably released from the astrocyte-like cells with subsequent activation of the neuronal NMDA receptors. The organization of the H 2 S-producing cell complexes suggests that the amount of glutamate produced in the trout cerebellum and its reuptake is controlled with the involvement of astrocyte-like cells, reducing its excitotoxicity. We believe that the increase in the number of H 2 S-producing cells constitutes a response to oxidative stress, and the overproduction of H 2 S neutralizes the reactive oxygen species.2 completely clarified thus far. H 2 S, like nitric oxide (NO), is known to mediate posttranslational modification of proteins by adding additional sulfur to reactive cysteine residues. This modification, referred to as S-sulfhydration, is required to activate or inactivate many classes of proteins, including the ion channels, such as the ATP-dependent potassium channels, TRPV3, TRPV6, TRPM [6], enzymes, and the transcription factors NF-kB and Nrf2 [7]. Modulation of ion channels, as well as the inflammatory and the antioxidant transcription factors, using H 2 S after traumatic brain injury, can play a significant role in reducing edema and inflammation [8].Recently, the involvement of H 2 S in cerebral ischemia, traumatic brain injury (TBI), and decrease in reactive oxygen species in the H 2 S-dependent mechanisms has been studied using different models [8][9][10]. The use of monoclonal antibodies against cystathionine β-synthase (CBS) in immunohistochemical (IHC) detection of the H 2 S-producing complexes in the brain of juvenile trout showed an increase in hydrogen sulfide production in different parts of the brain and CBS induction in the radial glia cells after the damage of the optic nerve [11]. It was shown that the toxic and/or neuroprotective effects of hydrogen sulfide depended on concentration: lower concentrations play a physiological role, while very high concentrations cause cell death [12,13]. Although hydrogen sulfide is considered a gasotransmitter, there is uncertainty about the total concentration of this volatile gas or highly active anionic particles (SH-) in both plasma and central nervous system tissues [14].The progress in studies of the hydrogen sulfide biology h...

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Section: Optic Tectumsupporting

confidence: 69%

Hydrogen Sulfide as a Factor of Neuroprotection during the Constitutive and Reparative Neurogenesis in Fish Brain

Пущина¹,

Вараксин²,

Обухов³

2020

Neuroprotection - New Approaches and Prospects

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“…Activation of microglial cells contributes to pathological development in many neurological diseases such as stroke, Alzheimer’s disease (AD) and Parkinson’s disease (PD). Inhibition of M1 microglial polarization and promotion of M2 polarization are considered as an important approach for the drug discovery and therapy of neurological and neurodegenerative disorders (Jin et al, 2014 ; Zhang et al, 2017b ). In the peripheral immune system, Sig-1R activation potently suppresses the inflammatory responses induced by a variety of stimuli (Bourrié et al, 2002 ).…”

Section: Sigma-1 Receptor and Microgliamentioning

confidence: 99%

Sigma-1 Receptor-Modulated Neuroinflammation in Neurological Diseases

Jia

Cheng

Wang

et al. 2018

Front. Cell. Neurosci.

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A large body of evidence indicates that sigma-1 receptors (Sig-1R) are important drug targets for a number of neuropsychiatric disorders. Sig-1Rs are enriched in central nervous system (CNS). In addition to neurons, both cerebral microglia and astrocytes express Sig-1Rs. Activation of Sig-1Rs is known to elicit potent neuroprotective effects and promote neuronal survival via multiple mechanisms, including promoting mitochondrial functions, decreasing oxidative stress and regulating neuroimmnological functions. In this review article, we focus on the emerging role of Sig-1Rs in regulating neuroinflammation and discuss the recent advances on the Sig-1R-modulating neuroinflammation in the pathophysiology and therapy of neurodegenerative disorders.

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“…4). Several reports described a proinflammatory activation of microglia by treatment with CM from neurons that underwent OGD [37][38][39][40], CM from endothelial cells after OGD [18], or microglia in a neuronal-microglia co-culture [41]. In contrast, the CM of OGD-pretreated astrocytes induces a mostly antiinflammatory phenotype in microglia [18,42]; however, a recent study also described the induction a proinflammatory phenotype [43].…”

Section: Discussionmentioning

confidence: 99%

Crosstalk between stressed brain cells: direct and indirect effects of ischemia and aglycemia on microglia

Rabenstein

Vay

Blaschke

et al. 2020

J Neuroinflammation

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Background: In cerebral ischemia, microglia have a dichotomous role in keeping the balance between pro-and anti-inflammatory mediators to avoid deleterious chronic inflammation and to leverage repair processes. Methods: We examined functional and inflammatory markers in primary rat microglia in vitro after oxygen-glucose deprivation (OGD) or glucose deprivation (aglycemia). We then investigated the preconditioning effect of OGD or aglycemia upon a subsequent strong inflammatory stimulus, here lipopolysaccharides (LPS). Moreover, an "in vitro brain model" of neurons and glia, differentiated from primary rat neural stem cells, was exposed to OGD or aglycemia. Conditioned medium (CM) of this neuronal/glial co-culture was then used to condition microglia, followed by LPS as a "second hit." Results: OGD or aglycemia at sublethal doses did not significantly affect microglia function, including the expression of inflammatory markers. However, preconditioning with either OGD or aglycemia led to a decreased pro-inflammatory response to a subsequent stimulus with LPS. Interestingly, the anti-inflammatory markers IGF-1 and IL-10 were additionally reduced after such preconditioning, while expression of CD206 remained unaffected. Treatment with CM from the neuronal/glial co-culture alone did not affect the expression of inflammatory markers in microglia. In contrast, treatment with CM increased the expression of both pro-and anti-inflammatory markers in microglia upon a second hit with LPS. Interestingly, this effect could be attenuated in microglia treated with CM from neuronal/glia co-cultures preconditioned with OGD or aglycemia.Conclusions: Data suggest specific and distinct microglia signatures in response to metabolic stress. While metabolic stress directly and indirectly applied to microglia did not mitigate their subsequent response to inflammation, preconditioning with metabolic stress factors such as OGD and aglycemia elicited a decreased inflammatory response to a subsequent inflammation stimulus.

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The cystathionine β-synthase/hydrogen sulfide pathway contributes to microglia-mediated neuroinflammation following cerebral ischemia

Cited by 71 publications

References 51 publications

Hydrogen Sulfide as a Factor of Neuroprotection during the Constitutive and Reparative Neurogenesis in Fish Brain

Hydrogen Sulfide as a Factor of Neuroprotection during the Constitutive and Reparative Neurogenesis in Fish Brain

Sigma-1 Receptor-Modulated Neuroinflammation in Neurological Diseases

Crosstalk between stressed brain cells: direct and indirect effects of ischemia and aglycemia on microglia

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