Role of interleukin‐6 and soluble IL‐6 receptor in region‐specific induction of astrocytic differentiation and neurotrophin expression

März, Pia; Heese, Klaus; Dimitriades-Schmutz, Beatrice; Rose-John, Stefan; Otten, U.

doi:10.1002/(sici)1098-1136(199905)26:3<191::aid-glia1>3.0.co;2-#

Cited by 159 publications

(106 citation statements)

References 55 publications

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“…DAMP signaling then leads to the activation of caspase 1, which in turn cleaves pro-IL-1 into active IL-1β (Walsh et al, 2014a). Upon activation by IL-1β, astrocytes can release large amounts of innate immune inflammatory mediators including several complement cascade proteins; cytokines including tumor necrosis factor (TNF), IL-1β, IL-6; and chemokines with CC (cysteine-cysteine) and CXC (cysteine-other amino acids-cysteine) motifs including CCL2, CXCL1, CXCL10, and CXCL12 (Bezzi et al, 2001;Fischer et al, 2014;Johnstone et al, 1999;Marz et al, 1999;Olmos and Llado, 2014;Santello and Volterra, 2012;Takahashi et al, 2003a;Torres-Platas et al, 2014b;Xie et al, 2003). This state is also associated with impaired glutamate clearance and oxidative stress, both of which contribute to excitotoxicity Tilleux and Hermans, 2007;Zou and Crews, 2005).…”

Section: Immune Regulationmentioning

confidence: 99%

“…Astrocytes respond to chronic CNS injuries and diseases by differentiating and proliferating into hypertrophic and/or migrating cell types-a term referred to as reactive astrocytosis (Khakh and Sofroniew, 2015;Liddelow and Barres, 2015;Sofroniew and Vinters, 2010). Reactive astrocytosis may have both reparative functions that preserve synaptic homeostasis (eg, increasing the secretion of neurotrophic factors such as nerve growth factor, brain-derived neurotrophic factor [BDNF], and activity-dependent neurotrophic growth factor, and increasing glutamate clearance through cradling and reuptake mechanisms) or toxic functions resulting in neuronal loss (Friedman et al, 1990;Liberto et al, 2004;Marz et al, 1999;Spranger et al, 1990). Accordingly, reactive astrocytes can be classified into A1 and A2 astrocytes (Karpuk et al, 2012).…”

Section: Immune Regulationmentioning

confidence: 99%

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

Haroon

Miller

Sanacora

2016

Neuropsychopharmacol

412

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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Section: Immune Regulationmentioning

confidence: 99%

Section: Immune Regulationmentioning

confidence: 99%

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

Haroon

Miller

Sanacora

2016

Neuropsychopharmacol

412

299

View full text Add to dashboard Cite

show abstract

“…While it has been suggested that astrocytes play a neuroprotective role in MS by inhibiting demyelination (Miljkovic et al, 2011), releasing anti-inflammatory cytokines (Bsibsi et al, 2006) and secreting proteins involved in myelin repair and neurotrophins to support regeneration of neurons (Marz et al, 1999, Moore et al, 2011a, Moore et al, 2011b, Mason et al, 2001, Miljkovic et al, 2011, it has also been proposed that astrocytes are detrimental in disease pathogenesis by releasing proinflammatory cytokines, contributing to BBB dysfunction (Argaw et al, 2006, Argaw et al, 2012 and preventing oligodendrocyte precursor cell (OPC) maturation into remyelinating oligodendrocytes (Messersmith et al, 2000, Sarchielli et al, 2008.…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiling of the astrocyte transcriptome in multiple sclerosis normal appearing white matter reveals a neuroprotective role

Waller

Woodroofe

Wharton

et al. 2016

Journal of Neuroimmunology

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“…ATP secreted by astrocytes into the extracellular space contributes to the regulation of postsynaptic efficiency at glutamatergic synapses (Gordon et al 2005). Also, astrocytes can produce neurotropic factors such as brain-derived neurotropic factor (BDNF) and nerve growth factor in response to damage, disease, or cytokines (Schwartz & Nishiyama 1994, Rudge et al 1995, Marz et al 1999, Albrecht et al 2002.…”

Section: Introductionmentioning

confidence: 99%

Astrocytes: new targets of melanocortin 4 receptor actions

Caruso¹,

Carniglia²,

Durand³

et al. 2013

Journal of Molecular Endocrinology

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Astrocytes exert a wide variety of functions with paramount importance in brain physiology. After injury or infection, astrocytes become reactive and they respond by producing a variety of inflammatory mediators that help maintain brain homeostasis. Loss of astrocyte functions as well as their excessive activation can contribute to disease processes; thus, it is important to modulate reactive astrocyte response. Melanocortins are peptides with well-recognized anti-inflammatory and neuroprotective activity. Although melanocortin efficacy was shown in systemic models of inflammatory disease, mechanisms involved in their effects have not yet been fully elucidated. Central anti-inflammatory effects of melanocortins and their mechanisms are even less well known, and, in particular, the effects of melanocortins in glial cells are poorly understood. Of the five known melanocortin receptors (MCRs), only subtype 4 is present in astrocytes. MC4R has been shown to mediate melanocortin effects on energy homeostasis, reproduction, inflammation, and neuroprotection and, recently, to modulate astrocyte functions. In this review, we will describe MC4R involvement in anti-inflammatory, anorexigenic, and anti-apoptotic effects of melanocortins in the brain. We will highlight MC4R action in astrocytes and discuss their possible mechanisms of action. Melanocortin effects on astrocytes provide a new means of treating inflammation, obesity, and neurodegeneration, making them attractive targets for therapeutic interventions in the CNS.

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Role of interleukin‐6 and soluble IL‐6 receptor in region‐specific induction of astrocytic differentiation and neurotrophin expression

Cited by 159 publications

References 55 publications

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

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

Gene expression profiling of the astrocyte transcriptome in multiple sclerosis normal appearing white matter reveals a neuroprotective role

Astrocytes: new targets of melanocortin 4 receptor actions

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