Astroglial IFITM3 mediates neuronal impairments following neonatal immune challenge in mice
Identifieur interne : 001181 ( Main/Exploration ); précédent : 001180; suivant : 001182Astroglial IFITM3 mediates neuronal impairments following neonatal immune challenge in mice
Auteurs : Daisuke Ibi [Japon] ; Taku Nagai [Japon] ; Akira Nakajima [Japon] ; Hiroyuki Mizoguchi [Japon] ; Takahiro Kawase [Japon] ; Daisuke Tsuboi [Japon] ; Shin-Ichi Kano [États-Unis] ; Yoshiaki Sato [Japon] ; Masahiro Hayakawa [Japon] ; Ulrike C. Lange [Royaume-Uni] ; David J. Adams [Royaume-Uni] ; M. Azim Surani [Royaume-Uni] ; Takaya Satoh [Japon] ; Akira Sawa [États-Unis] ; Kozo Kaibuchi [Japon] ; Toshitaka Nabeshima [Japon] ; Kiyofumi Yamada [Japon]Source :
- Glia [ 0894-1491 ] ; 2013-05.
English descriptors
- Teeft :
- Abnormality, Adult mice, Antiviral responses, Assay, Astrocyte, Astrocytes transfected, Axonal marker, Biol, Brain dysfunction, Cell type, Cell viability, Control astrocytes, Cos7, Cos7 cells, Cos7 cells transfected, Crucial role, Culture medium, Cultured, Cultured astrocytes, Cultured cells, Cultured neurons, Cytokine, Dendrite, Dendrite complexity, Dendrite length, Dendritic, Dendritic marker, Double immunostaining, Early endosomes, Early stages, Eea1, Endocytic, Endocytic activity, Endocytosis, Endosomes, Everitt, Exploratory preference, Expression levels, Extracellular humoral factors, Final treatment, Frontal cortex, Genotype, Hippocampal, Hippocampal neurons, Hippocampus, Humoral, Humoral factors, Ifitm3, Ifitm3 expression, Ifitm3 mrna, Immune, Immunostaining, Impairment, Independent experiments, Info, Inhibitory effects, Invitrogen, Laboratory animals, Map2, Map2 levels, Map2 protein levels, Middle panels, Mouse, Mrna, Mrna levels, Nagoya, Nagoya university, Nagoya university graduate school, Neonatal, Neonatal mice, Neonatal treatment, Neurite, Neurite elongation, Neurite outgrowth, Neurobasal medium, Neurodevelopment, Neurodevelopmental, Neurodevelopmental abnormalities, Neuron, Neuronal impairments, Neuropsychiatric diseases, Neurosci, Neutralizing antibody, Novel object, Novel objects, Present study, Primer, Protein levels, Puncta, Pyramidal neurons, Quantitative analysis, Receptor, Recycling, Representative images, Retention session, Rivero vaccari, Roche diagnostics gmbh, Schoggins, Sholl analysis, Significant difference, Spine density, Spine formation, Supp, Total neurite length, Training session, Transfected, Transfection, Transmembrane, Transmembrane protein, Tumor necrosis factor, Yount.
Abstract
Interferon‐induced transmembrane protein 3 (IFITM3) ıplays a crucial role in the antiviral responses of Type I interferons (IFNs). The role of IFITM3 in the central nervous system (CNS) is, however, largely unknown, despite the fact that its expression is increased in the brains of patients with neurologic and neuropsychiatric diseases. Here, we show the role of IFITM3 in long‐lasting neuronal impairments in mice following polyriboinosinic‐polyribocytidylic acid (polyI:C, a synthetic double‐stranded RNA)‐induced immune challenge during the early stages of development. We found that the induction of IFITM3 expression in the brain of mice treated with polyI:C was observed only in astrocytes. Cultured astrocytes were activated by polyI:C treatment, leading to an increase in the mRNA levels of inflammatory cytokines as well as Ifitm3. When cultured neurons were treated with the conditioned medium of polyI:C‐treated astrocytes (polyI:C‐ACM), neurite development was impaired. These polyI:C‐ACM‐induced neurodevelopmental abnormalities were alleviated by ifitm3−/− astrocyte‐conditioned medium. Furthermore, decreases of MAP2 expression, spine density, and dendrite complexity in the frontal cortex as well as memory impairment were evident in polyI:C‐treated wild‐type mice, but such neuronal impairments were not observed in ifitm3−/− mice. We also found that IFITM3 proteins were localized to the early endosomes of astrocytes following polyI:C treatment and reduced endocytic activity. These findings suggest that the induction of IFITM3 expression in astrocytes by the activation of the innate immune system during the early stages of development has non‐cell autonomous effects that affect subsequent neurodevelopment, leading to neuropathological impairments and brain dysfunction, by impairing endocytosis in astrocytes. GLIA 2013
Url:
DOI: 10.1002/glia.22461
Affiliations:
- Japon, Royaume-Uni, États-Unis
- Angleterre, Angleterre de l'Est, Maryland
- Cambridge
- Université de Cambridge
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Le document en format XML
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xml:lang="fr">Japon</country><wicri:regionArea>Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya</wicri:regionArea><wicri:noRegion>Nagoya</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, Meijo University, Nagoya</wicri:regionArea><wicri:noRegion>Nagoya</wicri:noRegion></affiliation></author><author><name sortKey="Nagai, Taku" sort="Nagai, Taku" uniqKey="Nagai T" first="Taku" last="Nagai">Taku Nagai</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya</wicri:regionArea><wicri:noRegion>Nagoya</wicri:noRegion></affiliation></author><author><name sortKey="Nakajima, Akira" sort="Nakajima, Akira" uniqKey="Nakajima A" first="Akira" 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first="Toshitaka" last="Nabeshima">Toshitaka Nabeshima</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, Meijo University, Nagoya</wicri:regionArea><wicri:noRegion>Nagoya</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Regional Pharmaceutical Care and Sciences, Faculty of Pharmacy, Meijo University, Nagoya</wicri:regionArea><wicri:noRegion>Nagoya</wicri:noRegion></affiliation></author><author><name sortKey="Yamada, Kiyofumi" sort="Yamada, Kiyofumi" uniqKey="Yamada K" first="Kiyofumi" last="Yamada">Kiyofumi Yamada</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, 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xml:lang="en"><term>Abnormality</term><term>Adult mice</term><term>Antiviral responses</term><term>Assay</term><term>Astrocyte</term><term>Astrocytes transfected</term><term>Axonal marker</term><term>Biol</term><term>Brain dysfunction</term><term>Cell type</term><term>Cell viability</term><term>Control astrocytes</term><term>Cos7</term><term>Cos7 cells</term><term>Cos7 cells transfected</term><term>Crucial role</term><term>Culture medium</term><term>Cultured</term><term>Cultured astrocytes</term><term>Cultured cells</term><term>Cultured neurons</term><term>Cytokine</term><term>Dendrite</term><term>Dendrite complexity</term><term>Dendrite length</term><term>Dendritic</term><term>Dendritic marker</term><term>Double immunostaining</term><term>Early endosomes</term><term>Early stages</term><term>Eea1</term><term>Endocytic</term><term>Endocytic activity</term><term>Endocytosis</term><term>Endosomes</term><term>Everitt</term><term>Exploratory preference</term><term>Expression levels</term><term>Extracellular humoral factors</term><term>Final treatment</term><term>Frontal cortex</term><term>Genotype</term><term>Hippocampal</term><term>Hippocampal neurons</term><term>Hippocampus</term><term>Humoral</term><term>Humoral factors</term><term>Ifitm3</term><term>Ifitm3 expression</term><term>Ifitm3 mrna</term><term>Immune</term><term>Immunostaining</term><term>Impairment</term><term>Independent experiments</term><term>Info</term><term>Inhibitory effects</term><term>Invitrogen</term><term>Laboratory animals</term><term>Map2</term><term>Map2 levels</term><term>Map2 protein levels</term><term>Middle panels</term><term>Mouse</term><term>Mrna</term><term>Mrna levels</term><term>Nagoya</term><term>Nagoya university</term><term>Nagoya university graduate school</term><term>Neonatal</term><term>Neonatal mice</term><term>Neonatal treatment</term><term>Neurite</term><term>Neurite elongation</term><term>Neurite outgrowth</term><term>Neurobasal medium</term><term>Neurodevelopment</term><term>Neurodevelopmental</term><term>Neurodevelopmental abnormalities</term><term>Neuron</term><term>Neuronal impairments</term><term>Neuropsychiatric diseases</term><term>Neurosci</term><term>Neutralizing antibody</term><term>Novel object</term><term>Novel objects</term><term>Present study</term><term>Primer</term><term>Protein levels</term><term>Puncta</term><term>Pyramidal neurons</term><term>Quantitative analysis</term><term>Receptor</term><term>Recycling</term><term>Representative images</term><term>Retention session</term><term>Rivero vaccari</term><term>Roche diagnostics gmbh</term><term>Schoggins</term><term>Sholl analysis</term><term>Significant difference</term><term>Spine density</term><term>Spine formation</term><term>Supp</term><term>Total neurite length</term><term>Training session</term><term>Transfected</term><term>Transfection</term><term>Transmembrane</term><term>Transmembrane protein</term><term>Tumor necrosis factor</term><term>Yount</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Interferon‐induced transmembrane protein 3 (IFITM3) ıplays a crucial role in the antiviral responses of Type I interferons (IFNs). The role of IFITM3 in the central nervous system (CNS) is, however, largely unknown, despite the fact that its expression is increased in the brains of patients with neurologic and neuropsychiatric diseases. Here, we show the role of IFITM3 in long‐lasting neuronal impairments in mice following polyriboinosinic‐polyribocytidylic acid (polyI:C, a synthetic double‐stranded RNA)‐induced immune challenge during the early stages of development. We found that the induction of IFITM3 expression in the brain of mice treated with polyI:C was observed only in astrocytes. Cultured astrocytes were activated by polyI:C treatment, leading to an increase in the mRNA levels of inflammatory cytokines as well as Ifitm3. When cultured neurons were treated with the conditioned medium of polyI:C‐treated astrocytes (polyI:C‐ACM), neurite development was impaired. These polyI:C‐ACM‐induced neurodevelopmental abnormalities were alleviated by ifitm3−/− astrocyte‐conditioned medium. Furthermore, decreases of MAP2 expression, spine density, and dendrite complexity in the frontal cortex as well as memory impairment were evident in polyI:C‐treated wild‐type mice, but such neuronal impairments were not observed in ifitm3−/− mice. We also found that IFITM3 proteins were localized to the early endosomes of astrocytes following polyI:C treatment and reduced endocytic activity. These findings suggest that the induction of IFITM3 expression in astrocytes by the activation of the innate immune system during the early stages of development has non‐cell autonomous effects that affect subsequent neurodevelopment, leading to neuropathological impairments and brain dysfunction, by impairing endocytosis in astrocytes. GLIA 2013</div></front></TEI><affiliations><list><country><li>Japon</li><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Angleterre de l'Est</li><li>Maryland</li></region><settlement><li>Cambridge</li></settlement><orgName><li>Université de Cambridge</li></orgName></list><tree><country name="Japon"><noRegion><name sortKey="Ibi, Daisuke" sort="Ibi, Daisuke" uniqKey="Ibi D" first="Daisuke" last="Ibi">Daisuke Ibi</name></noRegion><name sortKey="Hayakawa, Masahiro" sort="Hayakawa, Masahiro" uniqKey="Hayakawa M" first="Masahiro" last="Hayakawa">Masahiro Hayakawa</name><name sortKey="Ibi, Daisuke" sort="Ibi, Daisuke" uniqKey="Ibi D" first="Daisuke" last="Ibi">Daisuke Ibi</name><name sortKey="Kaibuchi, Kozo" sort="Kaibuchi, Kozo" uniqKey="Kaibuchi K" first="Kozo" last="Kaibuchi">Kozo Kaibuchi</name><name sortKey="Kaibuchi, Kozo" sort="Kaibuchi, Kozo" uniqKey="Kaibuchi K" first="Kozo" last="Kaibuchi">Kozo Kaibuchi</name><name sortKey="Kawase, Takahiro" sort="Kawase, Takahiro" uniqKey="Kawase T" first="Takahiro" last="Kawase">Takahiro Kawase</name><name sortKey="Mizoguchi, Hiroyuki" sort="Mizoguchi, Hiroyuki" uniqKey="Mizoguchi H" first="Hiroyuki" last="Mizoguchi">Hiroyuki Mizoguchi</name><name sortKey="Nabeshima, Toshitaka" sort="Nabeshima, Toshitaka" uniqKey="Nabeshima T" first="Toshitaka" last="Nabeshima">Toshitaka Nabeshima</name><name sortKey="Nabeshima, Toshitaka" sort="Nabeshima, Toshitaka" uniqKey="Nabeshima T" first="Toshitaka" last="Nabeshima">Toshitaka Nabeshima</name><name sortKey="Nagai, Taku" sort="Nagai, Taku" uniqKey="Nagai T" first="Taku" last="Nagai">Taku Nagai</name><name sortKey="Nakajima, Akira" sort="Nakajima, Akira" uniqKey="Nakajima A" first="Akira" last="Nakajima">Akira Nakajima</name><name sortKey="Sato, Yoshiaki" sort="Sato, Yoshiaki" uniqKey="Sato Y" first="Yoshiaki" last="Sato">Yoshiaki Sato</name><name sortKey="Satoh, Takaya" sort="Satoh, Takaya" uniqKey="Satoh T" first="Takaya" last="Satoh">Takaya Satoh</name><name sortKey="Tsuboi, Daisuke" sort="Tsuboi, Daisuke" uniqKey="Tsuboi D" first="Daisuke" last="Tsuboi">Daisuke Tsuboi</name><name sortKey="Yamada, Kiyofumi" sort="Yamada, Kiyofumi" uniqKey="Yamada K" first="Kiyofumi" last="Yamada">Kiyofumi Yamada</name><name sortKey="Yamada, Kiyofumi" sort="Yamada, Kiyofumi" uniqKey="Yamada K" first="Kiyofumi" last="Yamada">Kiyofumi Yamada</name><name sortKey="Yamada, Kiyofumi" sort="Yamada, Kiyofumi" uniqKey="Yamada K" first="Kiyofumi" last="Yamada">Kiyofumi Yamada</name></country><country name="États-Unis"><region name="Maryland"><name sortKey="Kano, Shin Chi" sort="Kano, Shin Chi" uniqKey="Kano S" first="Shin-Ichi" last="Kano">Shin-Ichi Kano</name></region><name sortKey="Sawa, Akira" sort="Sawa, Akira" uniqKey="Sawa A" first="Akira" last="Sawa">Akira Sawa</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Lange, Ulrike C" sort="Lange, Ulrike C" uniqKey="Lange U" first="Ulrike C." last="Lange">Ulrike C. Lange</name></region><name sortKey="Adams, David J" sort="Adams, David J" uniqKey="Adams D" first="David J." last="Adams">David J. Adams</name><name sortKey="Surani, M Azim" sort="Surani, M Azim" uniqKey="Surani M" first="M. Azim" last="Surani">M. Azim Surani</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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