PittsburghV1, Main, Exploration, bibRecord, 000088

Electrophilic nitro-fatty acids prevent astrocyte-mediated toxicity to motor neurons in a cell model of familial amyotrophic lateral sclerosis via nuclear factor erythroid 2-related factor activation.

Identifieur interne : 000088 ( Main/Exploration ); précédent : 000087; suivant : 000089

Electrophilic nitro-fatty acids prevent astrocyte-mediated toxicity to motor neurons in a cell model of familial amyotrophic lateral sclerosis via nuclear factor erythroid 2-related factor activation.

Auteurs : Pablo Diaz-Amarilla [Uruguay] ; Ernesto Miquel [Uruguay] ; Andrés Trostchansky [Uruguay] ; Emiliano Trias [Uruguay] ; Ana M. Ferreira [Uruguay] ; Bruce A. Freeman [États-Unis] ; Patricia Cassina [Uruguay] ; Luis Barbeito [Uruguay] ; Marcelo R. Vargas [États-Unis] ; Homero Rubbo [Uruguay]

Source :

Advances in Free Radical Biology & Medicine [ 8755-9668 ] ; 2016-03-22.

RBID : Hal:pasteur-01498339

English descriptors

mix :
- ALS, Astrocytes, Heme oxygenase, Motor neurons, Nitro-fatty acids, Nitroarachidonic acid, Nitrooleic acid, Nrf2.

Abstract

Nitro-fatty acids (NO2-FA) are electrophilic signaling mediators formed in tissues during inflammation, which are able to induce pleiotropic cytoprotective and antioxidant pathways including up regulation of Nuclear factor erythroid 2-related factor 2 (Nrf2) responsive genes. Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterized by the loss of motor neurons associated to an inflammatory process that usually aggravates the disease progression. In ALS animal models, the activation of the transcription factor Nrf2 in astrocytes confers protection to neighboring neurons. It is currently unknown whether NO2-FA can exert protective activity in ALS through Nrf2 activation. Herein we demonstrate that nitro-arachidonic acid (NO2-AA) or nitro-oleic acid (NO2-OA) administrated to astrocytes expressing the ALS-linked hSOD1(G93A) induce antioxidant phase II enzyme expression through Nrf2 activation concomitant with increasing intracellular glutathione levels. Furthermore, treatment of hSOD1(G93A)-expressing astrocytes with NO2-FA prevented their toxicity to motor neurons. Transfection of siRNA targeted to Nrf2 mRNA supported the involvement of Nrf2 activation in NO2-FA-mediated protective effects. Our results show for the first time that NO2-FA induce a potent Nrf2-dependent antioxidant response in astrocytes capable of preventing motor neurons death in a culture model of ALS.

Url:

https://hal-riip.archives-ouvertes.fr/pasteur-01498339

DOI: 10.1016/j.freeradbiomed.2016.03.013

Affiliations:

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

to stream Hal, to step Corpus: 000232
to stream Hal, to step Curation: 000232
to stream Hal, to step Checkpoint: 000087
to stream Main, to step Merge: 000088
to stream Main, to step Curation: 000088

Le document en format XML

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</author>
</analytic>
<idno type="DOI">10.1016/j.freeradbiomed.2016.03.013</idno>
<series><title level="j">Advances in Free Radical Biology & Medicine</title>
<idno type="ISSN">8755-9668</idno>
<imprint><date type="datePub">2016-03-22</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="mix" xml:lang="en"><term>ALS</term>
<term>Astrocytes</term>
<term>Heme oxygenase</term>
<term>Motor neurons</term>
<term>Nitro-fatty acids</term>
<term>Nitroarachidonic acid</term>
<term>Nitrooleic acid</term>
<term>Nrf2</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Nitro-fatty acids (NO2-FA) are electrophilic signaling mediators formed in tissues during inflammation, which are able to induce pleiotropic cytoprotective and antioxidant pathways including up regulation of Nuclear factor erythroid 2-related factor 2 (Nrf2) responsive genes. Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterized by the loss of motor neurons associated to an inflammatory process that usually aggravates the disease progression. In ALS animal models, the activation of the transcription factor Nrf2 in astrocytes confers protection to neighboring neurons. It is currently unknown whether NO2-FA can exert protective activity in ALS through Nrf2 activation. Herein we demonstrate that nitro-arachidonic acid (NO2-AA) or nitro-oleic acid (NO2-OA) administrated to astrocytes expressing the ALS-linked hSOD1(G93A) induce antioxidant phase II enzyme expression through Nrf2 activation concomitant with increasing intracellular glutathione levels. Furthermore, treatment of hSOD1(G93A)-expressing astrocytes with NO2-FA prevented their toxicity to motor neurons. Transfection of siRNA targeted to Nrf2 mRNA supported the involvement of Nrf2 activation in NO2-FA-mediated protective effects. Our results show for the first time that NO2-FA induce a potent Nrf2-dependent antioxidant response in astrocytes capable of preventing motor neurons death in a culture model of ALS.</div>
</front>
</TEI>
<affiliations><list><country><li>Uruguay</li>
<li>États-Unis</li>
</country>
<region><li>Pennsylvanie</li>
</region>
<settlement><li>Pittsburgh</li>
</settlement>
<orgName><li>Université de Pittsburgh</li>
</orgName>
</list>
<tree><country name="Uruguay"><noRegion><name sortKey="Diaz Amarilla, Pablo" sort="Diaz Amarilla, Pablo" uniqKey="Diaz Amarilla P" first="Pablo" last="Diaz-Amarilla">Pablo Diaz-Amarilla</name>
</noRegion>
<name sortKey="Barbeito, Luis" sort="Barbeito, Luis" uniqKey="Barbeito L" first="Luis" last="Barbeito">Luis Barbeito</name>
<name sortKey="Cassina, Patricia" sort="Cassina, Patricia" uniqKey="Cassina P" first="Patricia" last="Cassina">Patricia Cassina</name>
<name sortKey="Ferreira, Ana M" sort="Ferreira, Ana M" uniqKey="Ferreira A" first="Ana M" last="Ferreira">Ana M. Ferreira</name>
<name sortKey="Miquel, Ernesto" sort="Miquel, Ernesto" uniqKey="Miquel E" first="Ernesto" last="Miquel">Ernesto Miquel</name>
<name sortKey="Rubbo, Homero" sort="Rubbo, Homero" uniqKey="Rubbo H" first="Homero" last="Rubbo">Homero Rubbo</name>
<name sortKey="Trias, Emiliano" sort="Trias, Emiliano" uniqKey="Trias E" first="Emiliano" last="Trias">Emiliano Trias</name>
<name sortKey="Trostchansky, Andres" sort="Trostchansky, Andres" uniqKey="Trostchansky A" first="Andrés" last="Trostchansky">Andrés Trostchansky</name>
</country>
<country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Freeman, Bruce A" sort="Freeman, Bruce A" uniqKey="Freeman B" first="Bruce A" last="Freeman">Bruce A. Freeman</name>
</region>
<name sortKey="Vargas, Marcelo R" sort="Vargas, Marcelo R" uniqKey="Vargas M" first="Marcelo R" last="Vargas">Marcelo R. Vargas</name>
</country>
</tree>
</affiliations>
</record>

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Electrophilic nitro-fatty acids prevent astrocyte-mediated toxicity to motor neurons in a cell model of familial amyotrophic lateral sclerosis via nuclear factor erythroid 2-related factor activation.

Electrophilic nitro-fatty acids prevent astrocyte-mediated toxicity to motor neurons in a cell model of familial amyotrophic lateral sclerosis via nuclear factor erythroid 2-related factor activation.

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