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. 2021 Mar 26;12(4):326. doi: 10.1038/s41419-021-03494-1

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© The Author(s) 2021

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — A–B EdU (bar value = 100 μm) and colony formation assays depicted the proliferation of exosomes-activated HSCs with or without knockdown of SMO. C–E. Wound-healing (bar value = 80 μm) and transwell assays (bar value = 50 μm) unveiled the influence of silenced SMO on the migration and invasion capacity of exosomes-activated HSCs. F Western blot detected the levels of E-cadherin, N-cadherin, OCT4, and Nanog in exosomes-activated HSCs cells with or without SMO deficiency. G Sphere formation assay (bar value = 50 μm) uncovered the influence of silenced SMO on the stemness of activated HSCs. **P < 0.01.