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. 2021 Aug 10;18:176. doi: 10.1186/s12974-021-02227-7

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — CatH deficiency enhanced the proliferation of astrocytes in the hippocampus after HI. A, B Immunofluorescent CLSM images of GFAP (green) and Hoechst (blue) in the hippocampal CA1, CA3, and dentate gyrus (DG) regions of WT (A) and CatH^−/− (B) mice at 72 h after HI injury. Scale bar, 100 μm. C CLSM images of the astrocyte monolayers immune-stained by anti-GFAP antibody (green) with nuclear staining by Hoechst (blue) in the astrocyte monolayers 72 h after the scratch in the absence and presence of IFN-β. Dashed lines highlight the area that was damaged by the scratch. Scale bar, 50 μm. D Quantification of the migration of cultured astrocytes shown in (C). The gap width from three separate experiments was quantitatively evaluated using ImageJ software. The asterisks indicate a statistically significant difference from control group value (**p < 0.05, unpaired t test)