Medicinal Leech CNS as a Model for Exosome Studies in the Crosstalk between Microglia and Neurons

Raffo-Romero, Antonella; Arab, Tanina; Al-Amri, Issa; Marrec-Croq, Françoise Le; Camp, Christelle Van; Lemaire, Quentin; Salzet, Michel; Vizioli, Jacopo; Sautière, Pierre-Éric; Lefebvre, Christophe

doi:10.3390/ijms19124124

Cited by 27 publications

(30 citation statements)

References 60 publications

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“…Peripheral nerve injury signal is introduced into the central nervous system and chemical mediators are released from neurons. These chemical mediators induce the activation of glial cells, such as astrocytes and microglia [70,71,72]. Activated glial cells release chemokines and neuropeptides, which further influence neuronal activity.…”

Section: Discussionmentioning

confidence: 99%

Dose-Dependent Effect of Hyperbaric Oxygen Treatment on Burn-Induced Neuropathic Pain in Rats

Lee

Lin

et al. 2019

IJMS

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Hyperbaric oxygen treatment (HBOT) has been used to reduce neuropathic pain. Melatonin and opioid receptors are involved in neuropathic pain, but it is not known if HBOT works through these pathways to achieve its antinociceptive effect. We divided anesthetized rats into two treatment and three sham groups. The two treatment groups received third-degree burns on their right hind paws, one treated in a hyperbaric chamber for a week and the other for two weeks. We evaluated the mechanical paw-withdrawal threshold (MWT) and expression of melatonin receptor 1 (MT1), melatonin receptor 2 (MT2), μ (MOR) and κ (KOR) opioid receptor, brain-derived neurotrophic factor (BDNF), Substance P, and calcitonin gene-related peptide (CGRP) in cuneate nucleus, dorsal horn, and hind paw skin by immunohistochemical, immunofluorescence assays and real-time quantitative polymerase chain reaction (RT-PCR). The group receiving one-week HBOT had increased expressions of MT1, MT2, MOR and KOR and decreased expressions of BDNF, Substance P, and CGRP. Their mechanically measured pain levels returned to normal within a week and lasted three weeks. This anti-allodynia effect lasted twice as long in those treated for two weeks. Our findings suggest that increasing the duration of HBOT can reduce burn-induced mechanical allodynia for an extended period of time in rats. The upregulation of melatonin and opioid receptors observed after one week of HBOT suggests they may be partly involved in attenuation of the mechanical allodynia. Downregulation of BDNF, substance P and CGRP may have also contributed to the overall beneficial effect of HBOT.

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Section: Discussionmentioning

confidence: 99%

Dose-Dependent Effect of Hyperbaric Oxygen Treatment on Burn-Induced Neuropathic Pain in Rats

Lee

Lin

et al. 2019

IJMS

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“…These constructs were then co-transfected in NCH82 cells, each AltProt being co-transfected with TPM4 independently of the other AltProts. Staining was realized as in ( 59 ). Briefly, transiently transfected cells were grown on coverslips, and rinsed with PBS before fixation with 4% paraformaldehyde for 15 min at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Alternative proteins are functional regulators in cell reprogramming by PKA activation

Cardon

Franck

Coyaud

et al. 2020

Nucleic Acids Research

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It has been recently shown that many proteins are lacking from reference databases used in mass spectrometry analysis, due to their translation templated on alternative open reading frames. This questions our current understanding of gene annotation and drastically expands the theoretical proteome complexity. The functions of these alternative proteins (AltProts) still remain largely unknown. We have developed a large-scale and unsupervised approach based on cross-linking mass spectrometry (XL-MS) followed by shotgun proteomics to gather information on the functional role of AltProts by mapping them back into known signalling pathways through the identification of their reference protein (RefProt) interactors. We have identified and profiled AltProts in a cancer cell reprogramming system: NCH82 human glioma cells after 0, 16, 24 and 48 h Forskolin stimulation. Forskolin is a protein kinase A activator inducing cell differentiation and epithelial–mesenchymal transition. Our data show that AltMAP2, AltTRNAU1AP and AltEPHA5 interactions with tropomyosin 4 are downregulated under Forskolin treatment. In a wider perspective, Gene Ontology and pathway enrichment analysis (STRING) revealed that RefProts associated with AltProts are enriched in cellular mobility and transfer RNA regulation. This study strongly suggests novel roles of AltProts in multiple essential cellular functions and supports the importance of considering them in future biological studies.

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“…While some of these secreted factors may provide neurotrophic functions, pro-inflammatory factors exhibit deleterious effects [16,17] . Various neurotrophic secreted factors released from microglia induce neurite outgrowth and have been shown to be involved in regulating the cytoarchitecture of the developing brain [18][19][20] . Pro-inflammatory microglia, however, up-regulate cytokines and enzymes that produce reactive oxygen species, which have been implicated in axonal injury and disruption [16,[21][22][23][24][25][26][27][28][29][30][31][32] .…”

Section: Introductionmentioning

confidence: 99%

Microglial process convergence on axonal segments in health and disease

Benusa

Lafrenaye

2020

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Microglia dynamically interact with neurons influencing the development, structure, and function of neuronal networks. Recent studies suggest microglia may also influence neuronal activity by physically interacting with axonal domains responsible for action potential initiation and propagation. However, the nature of these microglial process interactions is not well understood. Microglial-axonal contacts are present early in development and persist through adulthood, implicating microglial interactions in the regulation of axonal integrity in both the developing and mature central nervous system. Moreover, changes in microglial-axonal contact have been described in disease states such as multiple sclerosis (MS) and traumatic brain injury (TBI). Depending on the disease state, there are increased associations with specific axonal segments. In MS, there is enhanced contact with the axon initial segment and node of Ranvier, while, in TBI, microglia alter interactions with axons at the site of injury, as well as at the axon initial segment. In this article, we review the interactions of microglial processes with axonal segments, analyzing their associations with various axonal domains and how these interactions may differ between MS and TBI. Furthermore, we discuss potential functional consequences and molecular mechanisms of these interactions and how these may differ among various types of microglial-axonal interactions.

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Medicinal Leech CNS as a Model for Exosome Studies in the Crosstalk between Microglia and Neurons

Cited by 27 publications

References 60 publications

Dose-Dependent Effect of Hyperbaric Oxygen Treatment on Burn-Induced Neuropathic Pain in Rats

Dose-Dependent Effect of Hyperbaric Oxygen Treatment on Burn-Induced Neuropathic Pain in Rats

Alternative proteins are functional regulators in cell reprogramming by PKA activation

Microglial process convergence on axonal segments in health and disease

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