Opposite regulation of metabotropic glutamate receptor 3 and metabotropic glutamate receptor 5 by inflammatory stimuli in cultured microglia and astrocytes

Berger, Julie; Dumont, Amélie; Focant, Michel; Vergouts, Maxime; Sternotte, Anthony; Calas, André-Guilhem; Goursaud, Stéphanie; Hermans, Emmanuel

doi:10.1016/j.neuroscience.2011.12.044

Cited by 40 publications

(33 citation statements)

References 52 publications

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“…We recently reported on the opposite regulation of these two receptors in astrocytes exposed to the inflammatory cytokines IL-1β or TNFα (Berger et al, 2012). Considering the distinct signalling pathways associated with these receptors, we hypothesised that the concomitant upregulation of mGluR3 and downregulation of mGluR5 could reinforce the neuroprotective activity of glial cells under inflammatory conditions.…”

Section: Discussionmentioning

confidence: 96%

“…It has since been shown that astrocytes play an essential role in mediating inflammatory processes in the brain and spinal cord (Dong and Benveniste, 2001;Moynagh, 2005). Astrocytes express receptors that recognise pathogenic molecules, such as toll-like receptors (TLR), and can directly respond to pro-inflammatory stimuli in-vitro (van Neerven et al, 2010a;Berger et al, 2012) or CNS-injuries in-vivo. Through constant interaction with microglial cells, astrocytes are involved in neuroinflammatory processes as they release both pro-and anti-inflammatory mediators.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Immunomodulatory influence of bone marrow-derived mesenchymal stem cells on neuroinflammation in astrocyte cultures

Schäfer

Calas

Vergouts

et al. 2012

Journal of Neuroimmunology

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Immunomodulatory influence of bone marrow-derived mesenchymal stem cells on neuroinflammation in astrocyte cultures

Schäfer

Calas

Vergouts

et al. 2012

Journal of Neuroimmunology

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“…Primary cultures were obtained from the cerebral cortices of newborn wild-type Wistar rats as described before [26]. In brief, cells were obtained by a sedimentation protocol and plated into 75 cm 2 poly-L-lysine-coated flasks.…”

Section: Methodsmentioning

confidence: 99%

Influence of intrathecal delivery of bone marrow-derived mesenchymal stem cells on spinal inflammation and pain hypersensitivity in a rat model of peripheral nerve injury

Schäfer

Berger

Deumens

et al. 2014

J Neuroinflammation

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BackgroundMultipotent mesenchymal stem (stromal) cells (MSCs) have been credited with immunomodulative properties, supporting beneficial outcomes when transplanted into a variety of disease models involving inflammation. Potential mechanisms include the secretion of paracrine factors and the establishment of a neurotrophic microenvironment. To test the hypothesis that MSCs release soluble mediators that can attenuate local inflammation, we here analysed the influence of MSCs on the activation of microglia cells, as well as on inflammatory parameters and pain behaviour in a surgical rat model of neuropathic pain.MethodsWe focussed on an experimental model of partial sciatic nerve ligation (PSNL), characterised by a rapid and persistent inflammation in the dorsal lumbar spinal cord where sensory inputs from the sciatic nerve are processed. Via indwelling intrathecal catheters, MSCs were repetitively grafted into the intrathecal lumbar space. Animals were evaluated for mechanical and thermal hypersensitivity over a period of 21 days after PSNL. Afterwards, spinal cords were processed for immunohistochemical analysis of the microglial marker ionized calcium-binding adapter molecule 1 (Iba1) and quantification of inflammatory markers in ipsilateral dorsal horns. We hypothesised that injections on postsurgical days 2 to 4 would interfere with microglial activation, leading to a reduced production of pro-inflammatory cytokines and amelioration of pain behaviour.ResultsPSNL-induced mechanical allodynia or heat hyperalgesia were not influenced by MSC transplantation, and spinal cord inflammatory processes remained largely unaffected. Indeed, the early microglial response to PSNL characterised by increased Iba1 expression in the lumbar dorsal horn was not significantly altered and cytokine levels in the spinal cord at 21 days after surgery were similar to those found in vehicle-injected animals. Grafted MSCs were detected close to the pia mater, but were absent within the spinal cord parenchyma.ConclusionsWe conclude that intrathecal administration is not an appropriate route to deliver cells for treatment of acute spinal cord inflammation as it leads to entrapment of grafted cells within the pia mater. We propose that the early inflammatory response triggered by PSNL in the lumbar spinal cord failed to effectively recruit MSCs or was insufficient to disturb the tissue integrity so as to allow MSCs to penetrate the spinal cord parenchyma.

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“…Cytokines, including the interleukins and tumor necrosis factor α, and neurotrophins, such as nerve growth factor (NGF), are also released and are intimately involved in the facilitation of inflammation 15. Other substances such as excitatory amino acids (glutamate) and opioids (endothelin-1) have also been implicated in the acute inflammatory response 16 17. Some of these agents may directly activate nociceptors, while others bring about the recruitment of other cells which then release further facilitatory agents 18.…”

Section: Basic Building Blocks Of Painmentioning

confidence: 99%

Why does my shoulder hurt? A review of the neuroanatomical and biochemical basis of shoulder pain

2013

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If a patient asks 'why does my shoulder hurt?' the conversation will quickly turn to scientific theory and sometimes unsubstantiated conjecture. Frequently, the clinician becomes aware of the limits of the scientific basis of their explanation, demonstrating the incompleteness of our understanding of the nature of shoulder pain. This review takes a systematic approach to help answer fundamental questions relating to shoulder pain, with a view to providing insights into future research and novel methods for treating shoulder pain. We shall explore the roles of (1) the peripheral receptors, (2) peripheral pain processing or 'nociception', (3) the spinal cord, (4) the brain, (5) the location of receptors in the shoulder and (6) the neural anatomy of the shoulder. We also consider how these factors might contribute to the variability in the clinical presentation, the diagnosis and the treatment of shoulder pain. In this way we aim to provide an overview of the component parts of the peripheral pain detection system and central pain processing mechanisms in shoulder pain that interact to produce clinical pain.

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Opposite regulation of metabotropic glutamate receptor 3 and metabotropic glutamate receptor 5 by inflammatory stimuli in cultured microglia and astrocytes

Cited by 40 publications

References 52 publications

Immunomodulatory influence of bone marrow-derived mesenchymal stem cells on neuroinflammation in astrocyte cultures

Immunomodulatory influence of bone marrow-derived mesenchymal stem cells on neuroinflammation in astrocyte cultures

Influence of intrathecal delivery of bone marrow-derived mesenchymal stem cells on spinal inflammation and pain hypersensitivity in a rat model of peripheral nerve injury

Why does my shoulder hurt? A review of the neuroanatomical and biochemical basis of shoulder pain

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