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. 2020 Jul 25;18:105. doi: 10.1186/s12951-020-00665-8

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© The Author(s) 2020

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. 9 — Overexpression of MYH9 abolishes the functional effects of miR-124-3p^OE-Exos on M1 microglia and A1 astrocytes. a ELISA assays were conducted to evaluate pro-inflammatory cytokines. Rescue experiments for miR-124-3p overexpression were carried out by the ectopic expression of MYH9 in microglia. M1 microglia and A1 astrocytes were detected by immunofluorescence (b, c) and western blot analysis (d, e). *P < 0.05 and ^#P < 0.05