Human T-Cell Lymphotropic Virus Type 1-Infected T Lymphocytes Impair Catabolism and Uptake of Glutamate by Astrocytes via Tax-1 and Tumor Necrosis Factor Alpha

Szymocha, Raphaël; Akaoka, H.; Dutuit, Magali; Malcus, Christophe; Didier-Bazes, M.; Belin, Marie‐Françoise; Giraudon, Pascale

doi:10.1128/jvi.74.14.6433-6441.2000

Cited by 74 publications

(58 citation statements)

References 70 publications

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“…TNF-␣ has been shown to inhibit glutamate uptake systems in astrocytes (Fine et al, 1996;Ye and Sontheimer, 1996;Szymocha et al, 2000), apparently at a post-translational level. In addition, TNF-␣ has been shown to upregulate either expression or function of transporters of different substrates (Durante et al, 1996;Gill et al, 1996;Irie et al, 1997;Mossner et al, 1998, Mochizuki et al, 2002.…”

Section: Discussionmentioning

confidence: 99%

In VitroIschemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway

Romera¹,

Hurtado²,

Botella³

et al. 2004

J. Neurosci.

117

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A short ischemic event [ischemic preconditioning (IPC)] can result in a subsequent resistance to severe ischemic injury (ischemic tolerance). Although tumor necrosis factor-␣ (TNF-␣) contributes to the brain damage found after cerebral ischemia, its expression and neuroprotective role in models of IPC have also been described. Regarding the role of TNF-␣ convertase (TACE/ADAM17), we have recently shown its upregulation in rat brain after IPC induced by transient middle cerebral artery occlusion and that subsequent TNF-␣ release accounts for at least part of the neuroprotection found in this model. We have now used an in vitro model of IPC using rat cortical cultures exposed to sublethal oxygen-glucose deprivation (OGD) to investigate TACE expression and activity after IPC and the subsequent mechanisms of ischemic tolerance. OGD-induced cell death was significantly reduced in cells exposed to IPC by sublethal OGD 24 hr before, an effect that was inhibited by the TACE inhibitor BB3103 (1 M) and anti-TNF-␣ antibody (2 g/ml) and that was mimicked by TNF-␣ (10 pg/ml) preincubation. Western blot analysis showed that TACE expression is increased after IPC. IPC caused TNF-␣ release, an effect that was blocked by the selective TACE inhibitor BB-3103. In addition, IPC diminished the increase in extracellular glutamate caused by OGD and increased cellular glutamate uptake and expression of EAAT2 and EAAT3 glutamate transporters; however, only EAAT3 upregulation was mediated by increased TNF-␣. These data demonstrate that neuroprotection induced by IPC involves upregulation of glutamate uptake partly mediated by TACE overexpression.

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Section: Discussionmentioning

confidence: 99%

In VitroIschemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway

Romera¹,

Hurtado²,

Botella³

et al. 2004

J. Neurosci.

117

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“…Exposure of astrocytes to recombinant HIV-1 envelope glycoprotein gp120 alters cell physiology (Benos et al, 1994a), including a potential e ect on glutamate transport as indicated by increased D-aspartate e ux in astrocytes treated with gp120 (Benos et al, 1994b). Impairment of glutamate transport was also observed after incubation of human astrocytes with TNF-a (Fine et al, 1996) or co-cultivation with T cells infected with human T cell leukemia virus type I (HTLVI) (Szymocha et al, 2000), and similar defects were found in feline astrocytes after infection with feline immunode®ciency virus (FIV) (Yu et al, 1998). More recent studies indicate that ligation of the HIV-1 coreceptor on astrocytes, CXCR4 by either stromal cell-derived factor 1 (SDF-1) or gp120 can stimulate a novel signaling pathway that involves Ca 2+ -dependent release of glutamate (Sharma and Vijayaraghavan, 2001) in a process including activation of the CXCR4 receptor, an autocrine/paracrine TNF-a-dependent signaling, and prostaglandin (Bezzi et al, 2001).…”

Section: Introductionmentioning

confidence: 96%

Identification and cloning of human astrocyte genes displaying elevated expression after infection with HIV-1 or exposure to HIV-1 envelope glycoprotein by rapid subtraction hybridization, RaSH

et al. 2002

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“…As mentioned previously, EAATs are expressed on astrocytes and oligodendrocyte cells both in resting and during activation states, whereas microglia express these transporters only when activated by immune factors such as LPS (Persson et al, 2005). Inflammatory molecules such as IL-1β and TNF released during immune activation suppress astrocytic expression of GLT-1 and GLAST glutamate transporters (similar to EAAT2 and EAAT1 in humans) in cell culture experiments (Korn et al, 2005;Szymocha et al, 2000;Wang et al, 2013a;Ye and Sontheimer, 1996), and EAAT2 expression is diminished in inflammatory CNS lesions of both laboratory animals and humans (Ohgoh et al, 2002;Vercellino et al, 2007). Several excellent reviews on this topic are available for further reference (Malarkey and Parpura, 2008;Ohgoh et al, 2002;Tavares et al, 2002;Tilleux and Hermans, 2007;Vercellino et al, 2007).…”

Section: Eaatsmentioning

confidence: 99%

Inflammation, Glutamate, and Glia: A Trio of Trouble in Mood Disorders

Haroon

Miller

Sanacora

2016

Neuropsychopharmacol

389

299

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Increasing data indicate that inflammation and alterations in glutamate neurotransmission are two novel pathways to pathophysiology in mood disorders. The primary goal of this review is to illustrate how these two pathways may converge at the level of the glia to contribute to neuropsychiatric disease. We propose that a combination of failed clearance and exaggerated release of glutamate by glial cells during immune activation leads to glutamate increases and promotes aberrant extrasynaptic signaling through ionotropic and metabotropic glutamate receptors, ultimately resulting in synaptic dysfunction and loss. Furthermore, glutamate diffusion outside the synapse can lead to the loss of synaptic fidelity and specificity of neurotransmission, contributing to circuit dysfunction and behavioral pathology. This review examines the fundamental role of glia in the regulation of glutamate, followed by a description of the impact of inflammation on glial glutamate regulation at the cellular, molecular, and metabolic level. In addition, the role of these effects of inflammation on glia and glutamate in mood disorders will be discussed along with their translational implications.

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Human T-Cell Lymphotropic Virus Type 1-Infected T Lymphocytes Impair Catabolism and Uptake of Glutamate by Astrocytes via Tax-1 and Tumor Necrosis Factor Alpha

Cited by 74 publications

References 70 publications

In VitroIschemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway

In VitroIschemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway

Identification and cloning of human astrocyte genes displaying elevated expression after infection with HIV-1 or exposure to HIV-1 envelope glycoprotein by rapid subtraction hybridization, RaSH

Inflammation, Glutamate, and Glia: A Trio of Trouble in Mood Disorders

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