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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: αVβ3 Integrin regulates astrocyte reactivity

Fig. 2

TNF pre-treatment enables Thy-1 signaling in primary astrocytes. a Representative western blot of β3 Integrin, Syndecan-4, P2X7R, Connexin-43, and Pannexin-1 after 48 h of treatment with TNF. Values indicate fold increase. b Localization of Connexin-43, Pannexin-1, Syndecan-4, and P2X7R in TNF-treated astrocytes and control cells (in green). Nuclei appear in blue. Magnification bar = 50 μm. c ATP measurements in the extracellular medium of primary astrocytes treated with Trail-R2-Fc or Thy-1-Fc for 10 min. Cells were previously treated, or not, with TNF for 48 h and incubated with the Connexin-blocking drug Heptanol (500 μM) and the Pannexin-blocking drug, Probenecid (1 mM). d Quantification of intracellular calcium levels in TNF-treated astrocytes stimulated with Thy-1-Fc and pre-treated with Heptanol and Probenecid or the P2X7R inhibitor BBG (5 μM). Trail-R2-Fc was used as a negative control. Values are 1.61 ± 0.27 for Thy-1+TNF, 1.08 ± 0.09 for Thy-1+TNF+BBG, 1.01 ± 0.02 for Thy-1+TNF+Pro-Hep, 1.06 ± 0.04 Trail-R2-Fc+TNF and 1.04 ± 0.04 for Thy-1 without TNF. e Wound-healing assay in rat primary astrocytes. After treatment with BBG (5 μM), Apyrase (3 UI/mL), or vehicle (PBS), cells were stimulated with Trail-R2-Fc, Thy-1-Fc for 24 h. Values shown are the means ± s.e.m. from three independent experiments. *p < 0.05

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