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. 2021 Feb 2;37(4):497–510. doi: 10.1007/s12264-020-00626-z

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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/.

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Fig. 8 — M2 phenotype microglial exosomes promote glioma growth in vivo. A Real-time qPCR was used to verify relative expression levels of Bmal1 and miR-7239-3p in tumor tissues. The internal reference genes were β-actin and U6, respectively. B Fitting curve of the correlation analysis between the relative expression levels of miR-7239-3p and Bmal1. C The subcutaneous tumor formation in nude mice. D The pathological morphology of glioma tissue after HE staining. Arrows indicate the fragmented nuclei (karyorrhexis). E The curve graph of tumor volume changes with time in each group. F The curve of mouse weight change with time in each group. G, H IHC was used to detect the expression of BMAL1 protein in each group. I The TUNEL apoptosis staining of each group. J The statistical analysis results of apoptosis index. K The tumor weight in each group (n = 6). *P < 0.05, **P < 0.01, ***P < 0.001.