P2Y12 Receptor on the Verge of a Neuroinflammatory Breakdown

In the CNS, neuroinflammation occurring during pathologies as amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) is the consequence of an intricate interplay orchestrated by various cell phenotypes. Among the molecular cues having a role in this process, extracellular nucleotides are re...

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Main Authors: Susanna Amadio, Chiara Parisi, Cinzia Montilli, Alberto Savio Carrubba, Savina Apolloni, Cinzia Volonté
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2014/975849
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author Susanna Amadio
Chiara Parisi
Cinzia Montilli
Alberto Savio Carrubba
Savina Apolloni
Cinzia Volonté
author_facet Susanna Amadio
Chiara Parisi
Cinzia Montilli
Alberto Savio Carrubba
Savina Apolloni
Cinzia Volonté
author_sort Susanna Amadio
collection DOAJ
description In the CNS, neuroinflammation occurring during pathologies as amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) is the consequence of an intricate interplay orchestrated by various cell phenotypes. Among the molecular cues having a role in this process, extracellular nucleotides are responsible for intercellular communication and propagation of inflammatory stimuli. This occurs by binding to several receptor subtypes, defined P2X/P2Y, which are widespread in different tissues and simultaneously localized on multiple cells. For instance, the metabotropic P2Y12 subtype is found in the CNS on microglia, affecting activation and chemotaxis, on oligodendrocytes, possessing a hypothesized role in myelination, and on astrocytes. By comparative analysis, we have established here that P2Y12 receptor immunolabelled by antibodies against C-terminus or second intracellular loop, is, respectively, distributed and modulated under neuroinflammatory conditions on ramified microglia or myelinated fibers, in primary organotypic cerebellar cultures, tissue slices from rat striatum and cerebellum, spinal cord sections from symptomatic/end stage SOD1-G93A ALS mice, and finally autoptic cortical tissue from progressive MS donors. We suggest that modulation of P2Y12 expression might play a dual role as analytic marker of branched/surveillant microglia and demyelinating lesions, thus potentially acquiring a predictive value under neuroinflammatory conditions as those found in ALS and MS.
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spelling doaj-art-1da9dfa59ee54ee8a1b2472803cc42c22025-08-20T03:54:38ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/975849975849P2Y12 Receptor on the Verge of a Neuroinflammatory BreakdownSusanna Amadio0Chiara Parisi1Cinzia Montilli2Alberto Savio Carrubba3Savina Apolloni4Cinzia Volonté5Santa Lucia Foundation, Via del Fosso di Fiorano 65, 00143 Rome, ItalyCellular Biology and Neurobiology Institute (CNR), Via del Fosso di Fiorano 65, 00143 Rome, ItalySanta Lucia Foundation, Via del Fosso di Fiorano 65, 00143 Rome, ItalySanta Lucia Foundation, Via del Fosso di Fiorano 65, 00143 Rome, ItalySanta Lucia Foundation, Via del Fosso di Fiorano 65, 00143 Rome, ItalySanta Lucia Foundation, Via del Fosso di Fiorano 65, 00143 Rome, ItalyIn the CNS, neuroinflammation occurring during pathologies as amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) is the consequence of an intricate interplay orchestrated by various cell phenotypes. Among the molecular cues having a role in this process, extracellular nucleotides are responsible for intercellular communication and propagation of inflammatory stimuli. This occurs by binding to several receptor subtypes, defined P2X/P2Y, which are widespread in different tissues and simultaneously localized on multiple cells. For instance, the metabotropic P2Y12 subtype is found in the CNS on microglia, affecting activation and chemotaxis, on oligodendrocytes, possessing a hypothesized role in myelination, and on astrocytes. By comparative analysis, we have established here that P2Y12 receptor immunolabelled by antibodies against C-terminus or second intracellular loop, is, respectively, distributed and modulated under neuroinflammatory conditions on ramified microglia or myelinated fibers, in primary organotypic cerebellar cultures, tissue slices from rat striatum and cerebellum, spinal cord sections from symptomatic/end stage SOD1-G93A ALS mice, and finally autoptic cortical tissue from progressive MS donors. We suggest that modulation of P2Y12 expression might play a dual role as analytic marker of branched/surveillant microglia and demyelinating lesions, thus potentially acquiring a predictive value under neuroinflammatory conditions as those found in ALS and MS.http://dx.doi.org/10.1155/2014/975849
spellingShingle Susanna Amadio
Chiara Parisi
Cinzia Montilli
Alberto Savio Carrubba
Savina Apolloni
Cinzia Volonté
P2Y12 Receptor on the Verge of a Neuroinflammatory Breakdown
Mediators of Inflammation
title P2Y12 Receptor on the Verge of a Neuroinflammatory Breakdown
title_full P2Y12 Receptor on the Verge of a Neuroinflammatory Breakdown
title_fullStr P2Y12 Receptor on the Verge of a Neuroinflammatory Breakdown
title_full_unstemmed P2Y12 Receptor on the Verge of a Neuroinflammatory Breakdown
title_short P2Y12 Receptor on the Verge of a Neuroinflammatory Breakdown
title_sort p2y12 receptor on the verge of a neuroinflammatory breakdown
url http://dx.doi.org/10.1155/2014/975849
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