ParkinsonCanadaV1, Main, Exploration, bibRecord, 001936

Mg2+ ions reduce microglial and THP-1 cell neurotoxicity by inhibiting Ca2+ entry through purinergic channels

Identifieur interne : 001936 ( Main/Exploration ); précédent : 001935; suivant : 001937

Mg2+ ions reduce microglial and THP-1 cell neurotoxicity by inhibiting Ca2+ entry through purinergic channels

Auteurs : Moonhee Lee [Canada] ; Nattinee Jantaratnotai [Canada] ; Edith Mcgeer [Canada] ; James G. Mclarnon [Canada] ; Patrick L. Mcgeer [Canada]

Source :

Brain research [ 0006-8993 ] ; 2011.

RBID : Pascal:11-0096108

Descripteurs français

Pascal (Inist)
- Microglie, Neurotoxicité, Calcium, Récepteur purinergique P2X7, Récepteur purinergique P2Y, Canal ionique, Démence d'Alzheimer, Maladie de Parkinson, Magnésium, Lignée cellulaire, In vitro, Neuroinflammation.
Wicri :
- topic : Calcium, Magnésium.

English descriptors

KwdEn :
- Alzheimer disease, Calcium, Cell line, In vitro, Ionic channel, Magnesium, Microglia, Neuroinflammation, Neurotoxicity, P2X7 purinergic receptor, P2Y purinergic receptor, Parkinson disease.

Abstract

Mg²⁺ is a known antagonist of some Ca²⁺ ion channels. It may therefore be able to counteract the toxic consequences of excessive Ca²⁺ entry into immune-type cells. Here we examined the effects of Mg²⁺ on inflammation induced by Ca²⁺ influx into microglia and THP-1 cells following activation of purinergic receptors. Using tissue culture, an inflammatory response was induced by treatment with either the P2X7 purinergic receptor agonist 2',3'-[benzoyl-4-benzoyl]-ATP (BzATP) or the P2Y2,4 receptor agonist uridine 5'-triphosphate (UTP). Both microglia and THP-1 cells expressed the mRNAs for these receptors. Treatment produced a rapid rise in intracellular Ca²⁺ which was significantly reduced by Mg²⁺ or the calcium chelator BAPTA-AM. Purinergic receptor stimulation activated the intracellular inflammatory pathway P38 MAP kinase and NFκB. This caused release of TNFα, IL-6, nitrite ions and other materials that are neurotoxic to SH-SY5Y cells. These effects were all ameliorated by Mg²⁺. They were also partly ameliorated by the P2X7R antagonists, oxATP and KN-62, the P2YR antagonist MRS2179, and the store operated Ca²⁺ channel blocker, SK96365. These results indicate that elevated Mg²⁺ is a broad spectrum inhibitor of Ca²⁺ entry into microglia or THP-1 cells. Mg²⁺ administration may be a strategy for reducing the damaging consequences Ca²⁺ induced neuroinflammation in degenerative neurological disorders such as Alzheimer disease and Parkinson disease.

Affiliations:

Canada

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Le document en format XML

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<term>Magnesium</term>
<term>Microglia</term>
<term>Neuroinflammation</term>
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<front><div type="abstract" xml:lang="en">Mg<sup>2+</sup>
 is a known antagonist of some Ca<sup>2+</sup>
 ion channels. It may therefore be able to counteract the toxic consequences of excessive Ca<sup>2+</sup>
 entry into immune-type cells. Here we examined the effects of Mg<sup>2+</sup>
 on inflammation induced by Ca<sup>2+</sup>
 influx into microglia and THP-1 cells following activation of purinergic receptors. Using tissue culture, an inflammatory response was induced by treatment with either the P2X7 purinergic receptor agonist 2',3'-[benzoyl-4-benzoyl]-ATP (BzATP) or the P2Y2,4 receptor agonist uridine 5'-triphosphate (UTP). Both microglia and THP-1 cells expressed the mRNAs for these receptors. Treatment produced a rapid rise in intracellular Ca<sup>2+</sup>
 which was significantly reduced by Mg<sup>2+</sup>
 or the calcium chelator BAPTA-AM. Purinergic receptor stimulation activated the intracellular inflammatory pathway P38 MAP kinase and NFκB. This caused release of TNFα, IL-6, nitrite ions and other materials that are neurotoxic to SH-SY5Y cells. These effects were all ameliorated by Mg<sup>2+</sup>
. They were also partly ameliorated by the P2X7R antagonists, oxATP and KN-62, the P2YR antagonist MRS2179, and the store operated Ca<sup>2+</sup>
 channel blocker, SK96365. These results indicate that elevated Mg<sup>2+</sup>
 is a broad spectrum inhibitor of Ca<sup>2+</sup>
 entry into microglia or THP-1 cells. Mg<sup>2+</sup>
 administration may be a strategy for reducing the damaging consequences Ca<sup>2+</sup>
 induced neuroinflammation in degenerative neurological disorders such as Alzheimer disease and Parkinson disease.</div>
</front>
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<tree><country name="Canada"><noRegion><name sortKey="Lee, Moonhee" sort="Lee, Moonhee" uniqKey="Lee M" first="Moonhee" last="Lee">Moonhee Lee</name>
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<name sortKey="Jantaratnotai, Nattinee" sort="Jantaratnotai, Nattinee" uniqKey="Jantaratnotai N" first="Nattinee" last="Jantaratnotai">Nattinee Jantaratnotai</name>
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<name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name>
<name sortKey="Mclarnon, James G" sort="Mclarnon, James G" uniqKey="Mclarnon J" first="James G." last="Mclarnon">James G. Mclarnon</name>
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Mg2+ ions reduce microglial and THP-1 cell neurotoxicity by inhibiting Ca2+ entry through purinergic channels

Mg2+ ions reduce microglial and THP-1 cell neurotoxicity by inhibiting Ca2+ entry through purinergic channels

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri