Platelet glutamate uptake and Th1 cells inversely correlate in relapsing/remitting and in progressive multiple sclerosis.


Journal

Multiple sclerosis and related disorders
ISSN: 2211-0356
Titre abrégé: Mult Scler Relat Disord
Pays: Netherlands
ID NLM: 101580247

Informations de publication

Date de publication:
Jun 2020
Historique:
received: 07 06 2019
revised: 06 02 2020
accepted: 10 02 2020
pubmed: 25 2 2020
medline: 23 3 2021
entrez: 25 2 2020
Statut: ppublish

Résumé

High affinity sodium-dependent Excitatory Amino Acid Transporters (EAAT), present in glial and neuron cells, clear around 90% of the synaptic cleft released glutamate, and their impaired activity seem to be critical for many neurodegenerative disorders, including Multiple Sclerosis (MS). These transporters are also present in human platelets, and they show molecular and biochemical characteristics similar to those in the CNS. The aim of this study was to investigate whether EAAT-dependent uptake is present also at the peripheral level in blood of MS patients. Moreover, since platelets (plt) and peripheral blood mononuclear cells (PBMC) share the same intra-corporeal fluid, they might be reciprocally influenced, and the glutamate uptake modulation might be useful as a peripheral "trait-marker" to characterize different clinical courses of MS RESULTS: : Reduced uptake values were found in MS patients compared to healthy controls (HC), as well as significant differences were found across MS clinical courses. Representative saturation curves showed that Vmax was significantly decreased for patients compared to HC. Conversely, dissociation constant of the two reactions appeared similar for MS and HC subjects. Furthermore, clinical forms of MS with mild (benign) prognosis was not affected as fa as concern EAAT uptake. Gender, age, and drug treatments did not impact glutamate uptake efficiency. Interestingly, a negative correlation between EAAT activity and percentage of Th1 cells (CD4+IFNγ+ and CD4+TBET+IFNγ+ cells) was observed, suggesting a relationship between EAAT impairment and a pro-inflammatory environment. Interestingly, as shown in the CNS, a relationship between clinical, inflammatory MS features and glutamate clearance can be also assessed in platelets. Moreover, glutamate uptake activity might be an useful biomarker to characterize patients with benign prognosis.

Sections du résumé

BACKGROUND BACKGROUND
High affinity sodium-dependent Excitatory Amino Acid Transporters (EAAT), present in glial and neuron cells, clear around 90% of the synaptic cleft released glutamate, and their impaired activity seem to be critical for many neurodegenerative disorders, including Multiple Sclerosis (MS). These transporters are also present in human platelets, and they show molecular and biochemical characteristics similar to those in the CNS.
OBJECTIVES OBJECTIVE
The aim of this study was to investigate whether EAAT-dependent uptake is present also at the peripheral level in blood of MS patients. Moreover, since platelets (plt) and peripheral blood mononuclear cells (PBMC) share the same intra-corporeal fluid, they might be reciprocally influenced, and the glutamate uptake modulation might be useful as a peripheral "trait-marker" to characterize different clinical courses of MS RESULTS: : Reduced uptake values were found in MS patients compared to healthy controls (HC), as well as significant differences were found across MS clinical courses. Representative saturation curves showed that Vmax was significantly decreased for patients compared to HC. Conversely, dissociation constant of the two reactions appeared similar for MS and HC subjects. Furthermore, clinical forms of MS with mild (benign) prognosis was not affected as fa as concern EAAT uptake. Gender, age, and drug treatments did not impact glutamate uptake efficiency. Interestingly, a negative correlation between EAAT activity and percentage of Th1 cells (CD4+IFNγ+ and CD4+TBET+IFNγ+ cells) was observed, suggesting a relationship between EAAT impairment and a pro-inflammatory environment.
CONCLUSIONS CONCLUSIONS
Interestingly, as shown in the CNS, a relationship between clinical, inflammatory MS features and glutamate clearance can be also assessed in platelets. Moreover, glutamate uptake activity might be an useful biomarker to characterize patients with benign prognosis.

Identifiants

pubmed: 32092504
pii: S2211-0348(20)30083-3
doi: 10.1016/j.msard.2020.102007
pii:
doi:

Substances chimiques

Glutamate Plasma Membrane Transport Proteins 0
Glutamic Acid 3KX376GY7L

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

102007

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest All the authors have no potential conflicts of interest relevant to this manuscript and they approve the manuscript. The research has been approved by the local ethics committee, in accordance with Helsinki Declaration.

Auteurs

Gironi M (G)

Institute of Experimental Neurology (INSpe); Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy; CAM-SYNLAB, Monza, Italy.

Dalla-Costa G (DC)

Institute of Experimental Neurology (INSpe); Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.

Frigo M (F)

Department of Neurology, S. Gerardo Hospital, Monza, Italy; Milan Center for Neuroscience, University of Milano-Bicocca, Milan, Italy.

Rovaris M (R)

IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy; Department of Pathophysiology and Transplantation, University of Milano, Milano, Italy.

Clerici M (C)

IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy.

Bazzini C (B)

Laboratory of Neurobiology, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy; Milan Center for Neuroscience, University of Milano-Bicocca, Milan, Italy.

Andreoni S (A)

Laboratory of Neurobiology, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy.

Comi G (C)

Institute of Experimental Neurology (INSpe); Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.

Furlan R (F)

Institute of Experimental Neurology (INSpe); Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.

Ferrarese C (F)

Department of Neurology, S. Gerardo Hospital, Monza, Italy; Laboratory of Neurobiology, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy; Milan Center for Neuroscience, University of Milano-Bicocca, Milan, Italy.

Cavaletti G (C)

Department of Neurology, S. Gerardo Hospital, Monza, Italy; Milan Center for Neuroscience, University of Milano-Bicocca, Milan, Italy; Experimental Neurology Unit, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy.

Saresella M (S)

IRCCS Fondazione Don Carlo Gnocchi, Milan, Italy.

Zoia Cp (Z)

Laboratory of Neurobiology, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy; Milan Center for Neuroscience, University of Milano-Bicocca, Milan, Italy. Electronic address: chiarapaola.zoia@unimib.it.

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