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. 2022 Jul 16;13:322. doi: 10.1186/s13287-022-03005-9

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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. 5 — miR-1208 is the key miRNA bind to METTL3 in EVs to exert anti-inflammatory effects. A. Western blot analysis of Ago-2 expression in hucMSCs lysates. B. Western blot analysis of IL-1β and cleaved caspase-1 levels in culture SN and pro-IL-1β, pro-caspase-1, NLRP3, and METTL3 levels in macrophage cell lysates in each group. C. Heat map of miRNA levels in hucMSCs-EVs (n = 3, Student’s t test). D. Four most significantly upregulated miRNAs in hucMSCs-EVs. E. The target sequence of miR-1208 estimated within 3′-UTR of METTL3. F. Western blot analysis of IL-1β and cleaved caspase-1 levels in culture SN and pro-IL-1β, pro-caspase-1, NLRP3, and METTL3 levels in macrophage cell lysates in each group. G. Luciferase reporter assay showing that METTL3 is the target gene for miR-1208 (n = 3, Student’s t test)