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. 2017 Jul 24;127(8):3136–3151. doi: 10.1172/JCI91301

Figure 1. Reactive astrocytes upregulate CLDN1, CLDN4, and JAM-A in vitro and in vivo.

Figure 1

(A and B) Western immunoblots (2 replicates depicted) (A) and mean values of densitometric quantification of immunoblot band intensities (from 3 biological replicates) (B) from cultured human astrocytes treated with 10 ng/ml IL-1β, IFN-γ, or TGF-β1 for 24 hours. CLDN1, CLDN4, and JAM-A are all induced by IL-1β, and CLDN1 and CLDN4 are also induced by TGF-β1. The TJ-associated protein tricellulin is induced by TGF-β1 alone. CLDN5 is not expressed by astrocytes. See also Supplemental Figure 1, A and B. (C) Following treatment with 10 ng/ml IL-1β, CLDN4 induction begins at 6 hours, is maintained at 24 and 48 hours, and decreases at 72 hours. (D) Immunostaining of human astrocyte cultures demonstrates that IL-1β induces expression of CLDN1, CLDN4, and JAM-A (red), which localize to the cell membranes of cells positive for the astrocyte marker GFAP. Scale bars: 20 μm. (E) In control C57BL/6 mice, cortical microinjection in vivo of adenovirus expressing IL-1 (AdIL-1), but not a control sequence, AdDL70 (AdCtrl), induces reactive astrocyte morphology and upregulation of CLDN1, CLDN4, and JAM-A at 7 days postinjection (7 dpi). Images are 3-dimensionally rendered projections. Scale bars: 40 μm. Data are representative of findings from 3 (A–C, and E) or more than 3 (D) biological replicates. *P < 0.05, **P < 0.01, ***P < 0.001.