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. 2022 Jul 13;13:291. doi: 10.1186/s13287-022-02963-4

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© The Author(s) 2022

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 TSG-6 suppressed ER stress by modulating the PI3K/AKT signaling pathway. a Representative images of GRP78-positive neurons in each experimental group. b Quantitative analysis of GRP78-positive neurons. c Expression of ER stress-related proteins as determined by Western blotting analysis. d, e Relative expression levels of ER stress-related proteins normalized to GAPDH. f Western blot analysis of AKT protein. g Relative expression levels of p-AKT normalized to GAPDH. *p < 0.05 compared with the SCIRI group, ^#p < 0.05 compared with the Lenti-Ctrl-sEVs group