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Background  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.    Methods  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.    Results  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.    Conclusions  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.    Electronic supplementary material  The online version of this article (10.1186/s12974-017-0968-5) contains supplementary material, which is available to authorized users.

αVβ3 Integrin regulates astrocyte reactivity