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. 2022 Jun 21;31:09636897221102898. doi: 10.1177/09636897221102898

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© The Author(s) 2022

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 6. — Schematic overview of the mechanisms whereby exosomes derived from ischemic heart extract-pretreated MSCs can promote HUVEC migration and proliferation. Ischemic heart extract-derived IL-22 can activate the IL22RA1/STAT3/DMBT1/VEGF pathway within MSCs. The activation of p-STAT3 also induced HIF-1α/β-catenin/VEGF pathway activation. HUVECs were then able to take up DMBT1 and VEGF-enriched MSC-Exos, with elevated DMBT1 levels promoting PI3K-Akt/GSK3β/β-catenin/VEGF signaling within these cells, thereby enhancing their migratory and proliferative activity. MSC: mesenchymal stem cell; HUVEC: human umbilical vein endothelial cell; HIF-1α: hypoxia inducible factor–1α; DMBT1: deleted in malignant brain tumors 1; VEGF: vascular endothelial growth factor.