Lagos-Cabré, RaúlAlvarez, AlvaroKong, MileneBurgos-Bravo, FrancescaCárdenas, AreliRojas-Mancilla, EdgardoPérez-Nuñez, RamónHerrera-Molina, RodrigoRojas, FabiolaSchneider, PascalHerrera-Marschitz, MarioQuest, Andrew F.G.van Zundert, BrigitteLeyton, Lisette2024-03-262024-03-262017-09Journal of Neuroinflammation Volume 14, Issue 129 September 2017 Article number 1941742-2094https://repositorio.unab.cl/handle/ria/55320Indexación: ScopusBackground: Neuroinflammation involves cytokine release, astrocyte reactivity and migration. Neuronal Thy-1 promotes DITNC1 astrocyte migration by engaging αVβ3 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. Methods: Wild-type rat astrocytes (TNF-activated) or from human SOD1G93A transgenic mice (a neurodegenerative disease model) were used to evaluate cell migration, Thy-1 receptor levels, signaling molecules, and reactivity markers. Results: Thy-1 induced astrocyte migration only after TNF priming. Increased expression of αVβ3 Integrin, Syndecan-4, P2X7R, Pannexin-1, Connexin-43, GFAP, and iNOS were observed in TNF-treated astrocytes. Silencing of β3 Integrin prior to TNF treatment prevented Thy-1-induced migration, while β3 Integrin over-expression was sufficient to induce astrocyte reactivity and allow Thy-1-induced migration. Finally, hSOD1G93A astrocytes behave as TNF-treated astrocytes since they were reactive and responsive to Thy-1. Conclusions: Therefore, inflammation induces expression of αVβ3 Integrin and other proteins, astrocyte reactivity, and Thy-1 responsiveness. Importantly, ectopic control of β3 Integrin levels modulates these responses regardless of inflammation. © 2017 The Author(s).enAmyotrophic lateral sclerosisCell migrationInflammationIntegrinsReactive astrocytesArtículo