α<sub>V</sub>β<sub>3</sub> Integrin regulates astrocyte reactivity.

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State: Public
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Serval ID
serval:BIB_7ECF79075A64
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
α<sub>V</sub>β<sub>3</sub> Integrin regulates astrocyte reactivity.
Journal
Journal of neuroinflammation
Author(s)
Lagos-Cabré R., Alvarez A., Kong M., Burgos-Bravo F., Cárdenas A., Rojas-Mancilla E., Pérez-Nuñez R., Herrera-Molina R., Rojas F., Schneider P., Herrera-Marschitz M., Quest AFG, van Zundert B., Leyton L.
ISSN
1742-2094 (Electronic)
ISSN-L
1742-2094
Publication state
Published
Issued date
29/09/2017
Peer-reviewed
Oui
Volume
14
Number
1
Pages
194
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Abstract
Neuroinflammation involves cytokine release, astrocyte reactivity and migration. Neuronal Thy-1 promotes DITNC1 astrocyte migration by engaging α <sub>V</sub> β <sub>3</sub> 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 <sup>G93A</sup> 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 <sub>V</sub> β <sub>3</sub> Integrin, Syndecan-4, P2X7R, Pannexin-1, Connexin-43, GFAP, and iNOS were observed in TNF-treated astrocytes. Silencing of β <sub>3</sub> Integrin prior to TNF treatment prevented Thy-1-induced migration, while β <sub>3</sub> Integrin over-expression was sufficient to induce astrocyte reactivity and allow Thy-1-induced migration. Finally, hSOD1 <sup>G93A</sup> astrocytes behave as TNF-treated astrocytes since they were reactive and responsive to Thy-1.
Therefore, inflammation induces expression of α <sub>V</sub> β <sub>3</sub> Integrin and other proteins, astrocyte reactivity, and Thy-1 responsiveness. Importantly, ectopic control of β <sub>3</sub> Integrin levels modulates these responses regardless of inflammation.
Keywords
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
Pubmed
Web of science
Open Access
Yes
Create date
23/10/2017 9:17
Last modification date
20/08/2019 14:39
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