ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000334

Interferon-γ-dependent cytotoxic activation of human astrocytes and astrocytoma cells

Identifieur interne : 000334 ( PascalFrancis/Corpus ); précédent : 000333; suivant : 000335

Interferon-γ-dependent cytotoxic activation of human astrocytes and astrocytoma cells

Auteurs : Sadayuki Hashioka ; Andis Klegeris ; Claudia Schwab ; Patrick L. Mcgeer

Source :

Neurobiology of aging [ 0197-4580 ] ; 2009.

RBID : Pascal:11-0160724

Descripteurs français

Pascal (Inist)
- Interféron gamma, Astrocyte, Récepteur biologique, Cytotoxicité, Sénescence, Maladie dégénérative, Homme.

English descriptors

KwdEn :
- Astrocyte, Biological receptor, Cytotoxicity, Degenerative disease, Gamma interferon, Human, Senescence.

Abstract

Astrocytes and microglia become activated in abroad spectrum of inflammatory neurodegenerative diseases. Activated microglia are widely believed to be the principal source of inflammation-induced neuronal degeneration in these disorders. To investigate the neurotoxic potential of human astrocytes, we exposed them and human astrocytic U-373 MG cells to a variety of inflammatory stimulants. We then assessed the effects of their supernatants on human SH-SY5 cells. When astrocytes and U-373 MG cells were stimulated with interferon (IFN)-γ (150 U/ml), their supernatants significantly reduced SH-SY5Y cell viability. Other powerful inflammatory stimulants such as lipopolysaccharide (0.5 μg/ml), tumor necrosis factor-α (10ng/ml) and interleukin-1β (lOng/ml), alone or in combination, were without effect. These combinations were also unable to enhance the IFN-γ effect. The induced cytotoxicities were reversed by JAK inhibitor I, a potent and specific inhibitor of JAKs. This result indicates that the neurotoxic effect was proceeding through the IFN-γ receptor (IFNGR)-JAK-STAT intracellular pathway. To establish that the IFNGR is expressed on both cultured astrocytes and U-373 MG cells, we performed RT-PCR on total RNA extracts to identify a specific IFNGR product. We showed the protein product on these cultured cells by immunocytochemistry using an antibody to IFNGR. Finally, using human postmortem material, we showed sharp upregulation of the IFNGR on activated astrocytes in affected areas in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. These findings suggest that activated astrocytes may become neurotoxic when stimulated by IFN-γ and may therefore exacerbate the pathology in a spectrum of neurodegenerative diseases.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A02	`01`			`@0 NEAGDO`
A03		`1`		`@0 Neurobiol. aging`
A05				`@2 30`
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A08	`01`	`1`	`ENG`	`@1 Interferon-γ-dependent cytotoxic activation of human astrocytes and astrocytoma cells`
A11	`01`	`1`		`@1 HASHIOKA (Sadayuki)`
A11	`02`	`1`		`@1 KLEGERIS (Andis)`
A11	`03`	`1`		`@1 SCHWAB (Claudia)`
A11	`04`	`1`		`@1 MCGEER (Patrick L.)`
A14	`01`			`@1 Kinsmen Laboratory of Neurological Research, Department of Psychiatry, The University of British Columbia, 2255 Wesbrook Mall @2 Vancouver, BC, V6T 1 W5 @3 CAN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut.`
A20				`@1 1924-1935`
A21				`@1 2009`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 20387 @5 354000194424420050`
A44				`@0 0000 @1 © 2011 INIST-CNRS. All rights reserved.`
A45				`@0 1 p.`
A47	`01`	`1`		`@0 11-0160724`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Neurobiology of aging`
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C01	`01`		`ENG`	@0 Astrocytes and microglia become activated in abroad spectrum of inflammatory neurodegenerative diseases. Activated microglia are widely believed to be the principal source of inflammation-induced neuronal degeneration in these disorders. To investigate the neurotoxic potential of human astrocytes, we exposed them and human astrocytic U-373 MG cells to a variety of inflammatory stimulants. We then assessed the effects of their supernatants on human SH-SY5 cells. When astrocytes and U-373 MG cells were stimulated with interferon (IFN)-γ (150 U/ml), their supernatants significantly reduced SH-SY5Y cell viability. Other powerful inflammatory stimulants such as lipopolysaccharide (0.5 μg/ml), tumor necrosis factor-α (10ng/ml) and interleukin-1β (lOng/ml), alone or in combination, were without effect. These combinations were also unable to enhance the IFN-γ effect. The induced cytotoxicities were reversed by JAK inhibitor I, a potent and specific inhibitor of JAKs. This result indicates that the neurotoxic effect was proceeding through the IFN-γ receptor (IFNGR)-JAK-STAT intracellular pathway. To establish that the IFNGR is expressed on both cultured astrocytes and U-373 MG cells, we performed RT-PCR on total RNA extracts to identify a specific IFNGR product. We showed the protein product on these cultured cells by immunocytochemistry using an antibody to IFNGR. Finally, using human postmortem material, we showed sharp upregulation of the IFNGR on activated astrocytes in affected areas in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. These findings suggest that activated astrocytes may become neurotoxic when stimulated by IFN-γ and may therefore exacerbate the pathology in a spectrum of neurodegenerative diseases.
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C03	`02`	`X`	`SPA`	`@0 Astrocito @5 02`
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C03	`03`	`X`	`ENG`	`@0 Biological receptor @5 03`
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C03	`04`	`X`	`ENG`	`@0 Cytotoxicity @5 04`
C03	`04`	`X`	`SPA`	`@0 Citotoxicidad @5 04`
C03	`05`	`X`	`FRE`	`@0 Sénescence @5 05`
C03	`05`	`X`	`ENG`	`@0 Senescence @5 05`
C03	`05`	`X`	`SPA`	`@0 Senescencia @5 05`
C03	`06`	`X`	`FRE`	`@0 Maladie dégénérative @5 09`
C03	`06`	`X`	`ENG`	`@0 Degenerative disease @5 09`
C03	`06`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 09`
C03	`07`	`X`	`FRE`	`@0 Homme @5 54`
C03	`07`	`X`	`ENG`	`@0 Human @5 54`
C03	`07`	`X`	`SPA`	`@0 Hombre @5 54`
C07	`01`	`X`	`FRE`	`@0 Névroglie @5 20`
C07	`01`	`X`	`ENG`	`@0 Neuroglia @5 20`
C07	`01`	`X`	`SPA`	`@0 Neuroglia @5 20`
N21				`@1 101`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 11-0160724 INIST
ET :	Interferon-γ-dependent cytotoxic activation of human astrocytes and astrocytoma cells
AU :	HASHIOKA (Sadayuki); KLEGERIS (Andis); SCHWAB (Claudia); MCGEER (Patrick L.)
AF :	Kinsmen Laboratory of Neurological Research, Department of Psychiatry, The University of British Columbia, 2255 Wesbrook Mall/Vancouver, BC, V6T 1 W5/Canada (1 aut., 2 aut., 3 aut., 4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Neurobiology of aging; ISSN 0197-4580; Coden NEAGDO; Royaume-Uni; Da. 2009; Vol. 30; No. 12; Pp. 1924-1935; Bibl. 1 p.
LA :	Anglais
EA :	Astrocytes and microglia become activated in abroad spectrum of inflammatory neurodegenerative diseases. Activated microglia are widely believed to be the principal source of inflammation-induced neuronal degeneration in these disorders. To investigate the neurotoxic potential of human astrocytes, we exposed them and human astrocytic U-373 MG cells to a variety of inflammatory stimulants. We then assessed the effects of their supernatants on human SH-SY5 cells. When astrocytes and U-373 MG cells were stimulated with interferon (IFN)-γ (150 U/ml), their supernatants significantly reduced SH-SY5Y cell viability. Other powerful inflammatory stimulants such as lipopolysaccharide (0.5 μg/ml), tumor necrosis factor-α (10ng/ml) and interleukin-1β (lOng/ml), alone or in combination, were without effect. These combinations were also unable to enhance the IFN-γ effect. The induced cytotoxicities were reversed by JAK inhibitor I, a potent and specific inhibitor of JAKs. This result indicates that the neurotoxic effect was proceeding through the IFN-γ receptor (IFNGR)-JAK-STAT intracellular pathway. To establish that the IFNGR is expressed on both cultured astrocytes and U-373 MG cells, we performed RT-PCR on total RNA extracts to identify a specific IFNGR product. We showed the protein product on these cultured cells by immunocytochemistry using an antibody to IFNGR. Finally, using human postmortem material, we showed sharp upregulation of the IFNGR on activated astrocytes in affected areas in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. These findings suggest that activated astrocytes may become neurotoxic when stimulated by IFN-γ and may therefore exacerbate the pathology in a spectrum of neurodegenerative diseases.
CC :	002A25L
FD :	Interféron gamma; Astrocyte; Récepteur biologique; Cytotoxicité; Sénescence; Maladie dégénérative; Homme
FG :	Névroglie
ED :	Gamma interferon; Astrocyte; Biological receptor; Cytotoxicity; Senescence; Degenerative disease; Human
EG :	Neuroglia
SD :	Interferón gamma; Astrocito; Receptor biológico; Citotoxicidad; Senescencia; Enfermedad degenerativa; Hombre
LO :	INIST-20387.354000194424420050
ID :	11-0160724

Links to Exploration step

Pascal:11-0160724

Le document en format XML

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<front><div type="abstract" xml:lang="en">Astrocytes and microglia become activated in abroad spectrum of inflammatory neurodegenerative diseases. Activated microglia are widely believed to be the principal source of inflammation-induced neuronal degeneration in these disorders. To investigate the neurotoxic potential of human astrocytes, we exposed them and human astrocytic U-373 MG cells to a variety of inflammatory stimulants. We then assessed the effects of their supernatants on human SH-SY5 cells. When astrocytes and U-373 MG cells were stimulated with interferon (IFN)-γ (150 U/ml), their supernatants significantly reduced SH-SY5Y cell viability. Other powerful inflammatory stimulants such as lipopolysaccharide (0.5 μg/ml), tumor necrosis factor-α (10ng/ml) and interleukin-1β (lOng/ml), alone or in combination, were without effect. These combinations were also unable to enhance the IFN-γ effect. The induced cytotoxicities were reversed by JAK inhibitor I, a potent and specific inhibitor of JAKs. This result indicates that the neurotoxic effect was proceeding through the IFN-γ receptor (IFNGR)-JAK-STAT intracellular pathway. To establish that the IFNGR is expressed on both cultured astrocytes and U-373 MG cells, we performed RT-PCR on total RNA extracts to identify a specific IFNGR product. We showed the protein product on these cultured cells by immunocytochemistry using an antibody to IFNGR. Finally, using human postmortem material, we showed sharp upregulation of the IFNGR on activated astrocytes in affected areas in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. These findings suggest that activated astrocytes may become neurotoxic when stimulated by IFN-γ and may therefore exacerbate the pathology in a spectrum of neurodegenerative diseases.</div>
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<ET>Interferon-γ-dependent cytotoxic activation of human astrocytes and astrocytoma cells</ET>
<AU>HASHIOKA (Sadayuki); KLEGERIS (Andis); SCHWAB (Claudia); MCGEER (Patrick L.)</AU>
<AF>Kinsmen Laboratory of Neurological Research, Department of Psychiatry, The University of British Columbia, 2255 Wesbrook Mall/Vancouver, BC, V6T 1 W5/Canada (1 aut., 2 aut., 3 aut., 4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neurobiology of aging; ISSN 0197-4580; Coden NEAGDO; Royaume-Uni; Da. 2009; Vol. 30; No. 12; Pp. 1924-1935; Bibl. 1 p.</SO>
<LA>Anglais</LA>
<EA>Astrocytes and microglia become activated in abroad spectrum of inflammatory neurodegenerative diseases. Activated microglia are widely believed to be the principal source of inflammation-induced neuronal degeneration in these disorders. To investigate the neurotoxic potential of human astrocytes, we exposed them and human astrocytic U-373 MG cells to a variety of inflammatory stimulants. We then assessed the effects of their supernatants on human SH-SY5 cells. When astrocytes and U-373 MG cells were stimulated with interferon (IFN)-γ (150 U/ml), their supernatants significantly reduced SH-SY5Y cell viability. Other powerful inflammatory stimulants such as lipopolysaccharide (0.5 μg/ml), tumor necrosis factor-α (10ng/ml) and interleukin-1β (lOng/ml), alone or in combination, were without effect. These combinations were also unable to enhance the IFN-γ effect. The induced cytotoxicities were reversed by JAK inhibitor I, a potent and specific inhibitor of JAKs. This result indicates that the neurotoxic effect was proceeding through the IFN-γ receptor (IFNGR)-JAK-STAT intracellular pathway. To establish that the IFNGR is expressed on both cultured astrocytes and U-373 MG cells, we performed RT-PCR on total RNA extracts to identify a specific IFNGR product. We showed the protein product on these cultured cells by immunocytochemistry using an antibody to IFNGR. Finally, using human postmortem material, we showed sharp upregulation of the IFNGR on activated astrocytes in affected areas in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. These findings suggest that activated astrocytes may become neurotoxic when stimulated by IFN-γ and may therefore exacerbate the pathology in a spectrum of neurodegenerative diseases.</EA>
<CC>002A25L</CC>
<FD>Interféron gamma; Astrocyte; Récepteur biologique; Cytotoxicité; Sénescence; Maladie dégénérative; Homme</FD>
<FG>Névroglie</FG>
<ED>Gamma interferon; Astrocyte; Biological receptor; Cytotoxicity; Senescence; Degenerative disease; Human</ED>
<EG>Neuroglia</EG>
<SD>Interferón gamma; Astrocito; Receptor biológico; Citotoxicidad; Senescencia; Enfermedad degenerativa; Hombre</SD>
<LO>INIST-20387.354000194424420050</LO>
<ID>11-0160724</ID>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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Interferon-γ-dependent cytotoxic activation of human astrocytes and astrocytoma cells

Interferon-γ-dependent cytotoxic activation of human astrocytes and astrocytoma cells

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