ParkinsonCanadaV1, PascalFrancis, Checkpoint, bibRecord, 000255

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

Identifieur interne : 000255 ( PascalFrancis/Checkpoint ); précédent : 000254; suivant : 000256

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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Pascal:11-0096108

Le document en format XML

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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>
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 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>
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<fC07 i1="02" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Pathologie du   système nerveux</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du   système nerveux central</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>25</s5>
</fC07>
<fN21><s1>059</s1>
</fN21>
</pA>
</standard>
</inist>
<affiliations><list><country><li>Canada</li>
</country>
</list>
<tree><country name="Canada"><noRegion><name sortKey="Lee, Moonhee" sort="Lee, Moonhee" uniqKey="Lee M" first="Moonhee" last="Lee">Moonhee Lee</name>
</noRegion>
<name sortKey="Jantaratnotai, Nattinee" sort="Jantaratnotai, Nattinee" uniqKey="Jantaratnotai N" first="Nattinee" last="Jantaratnotai">Nattinee Jantaratnotai</name>
<name sortKey="Mcgeer, Edith" sort="Mcgeer, Edith" uniqKey="Mcgeer E" first="Edith" last="Mcgeer">Edith Mcgeer</name>
<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>
</country>
</tree>
</affiliations>
</record>

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

This area was generated with Dilib version V0.6.29.
Data generation: Thu May 4 22:20:19 2017. Site generation: Fri Dec 23 23:17:26 2022

	La maladie de Parkinson au Canada (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

La maladie de Parkinson au Canada (serveur d'exploration)

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

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