Modulation of glial cell functions by adenosine receptors

Daré, Elisabetta; Schulte, Gunnar; Karovic, Olga; Hammarberg, Christian; Fredholm, Bertil B.

doi:10.1016/j.physbeh.2007.05.031

Cited by 126 publications

(84 citation statements)

References 48 publications

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“…Even if CXCR6 is expressed both on glia and neurons, we found that astrocytes are the essential players in CXCL16-induced effect, releasing soluble factor(s), such as CCL2, that mediate protection on neighboring neurons. Our data are in accordance with previous evidence that A 3 R is functionally expressed on astrocytes (Di Iorio et al, 2002), and that A 3 R modulates CCL2 release form astrocytes (Wittendorp et al, 2004), thus confirming that the modulation of glial function by ADO is an important issue in neuroprotection, and that ARs expressed on astrocytes control the release of neuroactive substances (Daré et al, 2007). Indeed, we have shown that ␣CCL2 neutralizing antibody significantly reduced CXCL16 neuroprotection.…”

Section: Discussionsupporting

confidence: 92%

CXCL16 Orchestrates Adenosine A₃Receptor and MCP-1/CCL2 Activity to Protect Neurons from Excitotoxic Cell Death in the CNS

Rosito¹,

Deflorio²,

Limatola³

et al. 2012

J. Neurosci.

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A role for chemokines as molecules mediating neuron-glia cross talk has emerged in recent years, both in physiological and pathological conditions. We demonstrate here for the first time that the chemokine CXCL16 and its unique receptor CXCR6 are functionally expressed in the CNS, and induce neuroprotection against excitotoxic damage due to excessive glutamate (Glu) exposure and oxygen glucose deprivation (OGD). In mice and rats we found that, to exert neuroprotection, CXCL16 requires the presence of extracellular adenosine (ADO), and that pharmacological or genetic inactivation of the ADO A 3 receptor, A 3 R, prevents CXCL16 effect. In experiments with astrocytes cocultured with cxcr6 gfp/gfp hippocampal cells, we demonstrate that CXCL16 acts directly on astrocytes to release soluble factors that are essential to mediate neuroprotection. In particular, we report that (1) upon stimulation with CXCL16 astrocytes release monocyte chemoattractant protein-1/CCL2 and (2) the neuroprotective effect of CXCL16 is reduced in the presence of neutralizing CCL2 antibody. In conclusion, we found that chemokine CXCL16 is able to mediate cross talk between astrocytes and neighboring neurons and, in pathological conditions such as excessive Glu or OGD exposure, is able to counteract neuronal cell death through an ADO-dependent chemokine-induced chemokine-release mechanism.

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Section: Discussionsupporting

confidence: 92%

CXCL16 Orchestrates Adenosine A₃Receptor and MCP-1/CCL2 Activity to Protect Neurons from Excitotoxic Cell Death in the CNS

Rosito¹,

Deflorio²,

Limatola³

et al. 2012

J. Neurosci.

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“…Extracellular ATP is initially converted by ectonucleotidases to ADP or AMP, which are further hydrolyzed to adenosine (Zimmermann, 1994). Adenosine is a signaling molecule that regulates cellular activity in the CNS through P1 purinergic receptor (Kaster et al, 2004;Daré et al, 2007). To exclude the effect of adenosine, we used ATP␥S, a nonhydrolyzable ATP analog.…”

Section: Discussionmentioning

confidence: 99%

Astrocyte-Originated ATP Protects Aβ_1-42-Induced Impairment of Synaptic Plasticity

Jung¹,

An²,

Hong³

et al. 2012

J. Neurosci.

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Activated microglia and reactive astrocytes are commonly found in and around the senile plaque, which is the central pathological hallmark of Alzheimer's disease. Astrocytes respond to neuronal activity through the release of gliotransmitters such as glutamate, D-serine, and ATP. However, it is largely unknown whether and how gliotransmitters affect neuronal functions. In this study, we explored the effect of a gliotransmitter, ATP, on neurons damaged by ␤-amyloid peptide (A␤). We found that A␤ 1-42 (A␤42) increased the release of ATP in cultures of primary astrocytes and U373 astrocyte cell line. We also found that exogenous ATP protected A␤42-mediated reduction in synaptic molecules, such as NMDA receptor 2A and PSD-95, through P2 purinergic receptors and prevented A␤42-induced spine reduction in cultured primary hippocampal neurons. Moreover, ATP prevented A␤42-induced impairment of long-term potentiation in acute hippocampal slices. Our findings suggest that A␤-induced release of gliotransmitter ATP plays a protective role against A␤42-mediated disruption of synaptic plasticity.

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“…They reveal novel insight into its functional involvement in endothelial and fluid transport; endothelial barrier function; adaption to hypoxia and ischemic preconditioning; the cardiovascular system; lung, liver, and kidney function [184,[217][218][219][220][221]; the airways [222]; immunity and inflammation [223,224]; leucocyte trafficking [225]; the nervous system [226,227], including a novel role of eN in inhibiting nociception [228]; or the immune control of cancer [229][230][231][232]. eN is a component of the multiresistance machinery of tumor cells against immune surveillance and/or anticancer therapy [233].…”

Section: Ecto-5′-nucleotidasementioning

confidence: 99%

Cellular function and molecular structure of ecto-nucleotidases

Zimmermann

Zebisch

Sträter

2012

Purinergic Signalling

872

922

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Ecto-nucleotidases play a pivotal role in purinergic signal transmission. They hydrolyze extracellular nucleotides and thus can control their availability at purinergic P2 receptors. They generate extracellular nucleosides for cellular reuptake and salvage via nucleoside transporters of the plasma membrane. The extracellular adenosine formed acts as an agonist of purinergic P1 receptors. They also can produce and hydrolyze extracellular inorganic pyrophosphate that is of major relevance in the control of bone mineralization. This review discusses and compares four major groups of ectonucleotidases: the ecto-nucleoside triphosphate diphosphohydrolases, ecto-5′-nucleotidase, ecto-nucleotide pyrophosphatase/phosphodiesterases, and alkaline phosphatases. Only recently and based on crystal structures, detailed information regarding the spatial structures and catalytic mechanisms has become available for members of these four ecto-nucleotidase families. This permits detailed predictions of their catalytic mechanisms and a comparison between the individual enzyme groups. The review focuses on the principal biochemical, cell biological, catalytic, and structural properties of the enzymes and provides brief reference to tissue distribution, and physiological and pathophysiological functions.

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Modulation of glial cell functions by adenosine receptors

Cited by 126 publications

References 48 publications

CXCL16 Orchestrates Adenosine A₃Receptor and MCP-1/CCL2 Activity to Protect Neurons from Excitotoxic Cell Death in the CNS

CXCL16 Orchestrates Adenosine A₃Receptor and MCP-1/CCL2 Activity to Protect Neurons from Excitotoxic Cell Death in the CNS

Astrocyte-Originated ATP Protects Aβ_1-42-Induced Impairment of Synaptic Plasticity

Cellular function and molecular structure of ecto-nucleotidases

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Modulation of glial cell functions by adenosine receptors

Cited by 126 publications

References 48 publications

CXCL16 Orchestrates Adenosine A3Receptor and MCP-1/CCL2 Activity to Protect Neurons from Excitotoxic Cell Death in the CNS

CXCL16 Orchestrates Adenosine A3Receptor and MCP-1/CCL2 Activity to Protect Neurons from Excitotoxic Cell Death in the CNS

Astrocyte-Originated ATP Protects Aβ1-42-Induced Impairment of Synaptic Plasticity

Cellular function and molecular structure of ecto-nucleotidases

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Product

Resources

About

CXCL16 Orchestrates Adenosine A₃Receptor and MCP-1/CCL2 Activity to Protect Neurons from Excitotoxic Cell Death in the CNS

CXCL16 Orchestrates Adenosine A₃Receptor and MCP-1/CCL2 Activity to Protect Neurons from Excitotoxic Cell Death in the CNS

Astrocyte-Originated ATP Protects Aβ_1-42-Induced Impairment of Synaptic Plasticity