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. Author manuscript; available in PMC: 2024 Feb 1.
Published in final edited form as: Glia. 2022 Oct 27;71(2):450–466. doi: 10.1002/glia.24286

Figure 10. Deletion of astrocytic YY1 regulates proinflammatory cytokine TNF-α and chemokine CXCL10 in the brain.

Figure 10.

(A-B) Coronal sections of brain tissues were immunostained with GFAP, Iba1, TNF-α, and CXCL10. The expression of GFAP, Iba1, and TNF-α/CXCL10 were shown as green, magenta, and red fluorescence signals, respectively, in the cortex, midbrain, and cerebellum of the WT and YY1 cKO mouse brain (×40 magnification with a confocal microscope, scale represent 50 μm). (C-D) Cortex, midbrain, and cerebellum regions were processed for TNF-α and CXCL10 by western blotting. (E) Human H4 astrocytes were transduced with shRNA lentiviral particles for YY1 knockdown and control, followed by detection and quantification of the proteins TNF-α and CXCL10. β-actin was used as a loading control for protein. ***, p<0.001; ****, p<0.0001 compared with the control (WT) (Student t-test, n = 3). Data are expressed as mean ± SD.