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Journal Article
αVβ3 Integrin regulates astrocyte reactivity
2017
Overview
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.
Publisher
BioMed Central,BioMed Central Ltd,BMC
Subject
