αVβ3 Integrin regulates astrocyte reactivity.

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Date

29 septembre 2017

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Périmètre
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Serveur académique Lausannois

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Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1186/s12974-017-0968-5

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/28962574

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1742-2094

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_7ECF79075A641

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Serveur Académique Lausannois

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Université de Lausanne et CHUV

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info:eu-repo/semantics/openAccess , Copying allowed only for non-profit organizations , https://serval.unil.ch/disclaimer

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Animals; Animals, Genetically Modified; Animals, Newborn; Astrocytes/drug effects; Astrocytes/physiology; Cell Movement/drug effects; Cell Movement/genetics; Cell Movement/physiology; Cells, Cultured; Connexins/genetics; Connexins/metabolism; Disease Models, Animal; Gene Expression Regulation/drug effects; Gene Expression Regulation/genetics; Humans; Integrin alphaVbeta3/genetics; Integrin alphaVbeta3/metabolism; Mice; Nerve Tissue Proteins/genetics; Nerve Tissue Proteins/metabolism; Neurodegenerative Diseases/genetics; Neurodegenerative Diseases/pathology; Rats; Receptors, Purinergic P2/genetics; Receptors, Purinergic P2/metabolism; Signal Transduction/drug effects; Signal Transduction/genetics; Superoxide Dismutase/genetics; Superoxide Dismutase/metabolism; Thy-1 Antigens/pharmacology; Tumor Necrosis Factor-alpha/pharmacology; Wound Healing/physiology; Amyotrophic lateral sclerosis; Cell migration; Inflammation; Integrins; Reactive astrocytes

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Glia (Neurology)

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R. Lagos-Cabré et al., « αVβ3 Integrin regulates astrocyte reactivity. », Serveur académique Lausannois, ID : 10.1186/s12974-017-0968-5

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Neuroinflammation involves cytokine release, astrocyte reactivity and migration. Neuronal Thy-1 promotes DITNC1 astrocyte migration by engaging α V β 3 Integrin and Syndecan-4. Primary astrocytes express low levels of these receptors and are unresponsive to Thy-1; thus, inflammation and astrocyte reactivity might be necessary for Thy-1-induced responses. Wild-type rat astrocytes (TNF-activated) or from human SOD1 G93A transgenic mice (a neurodegenerative disease model) were used to evaluate cell migration, Thy-1 receptor levels, signaling molecules, and reactivity markers. Thy-1 induced astrocyte migration only after TNF priming. Increased expression of α V β 3 Integrin, Syndecan-4, P2X7R, Pannexin-1, Connexin-43, GFAP, and iNOS were observed in TNF-treated astrocytes. Silencing of β 3 Integrin prior to TNF treatment prevented Thy-1-induced migration, while β 3 Integrin over-expression was sufficient to induce astrocyte reactivity and allow Thy-1-induced migration. Finally, hSOD1 G93A astrocytes behave as TNF-treated astrocytes since they were reactive and responsive to Thy-1. Therefore, inflammation induces expression of α V β 3 Integrin and other proteins, astrocyte reactivity, and Thy-1 responsiveness. Importantly, ectopic control of β 3 Integrin levels modulates these responses regardless of inflammation.

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