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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 4. — DMBT1 mediates the pro-angiogenic effects of MSC^E-Exos. (A) Western blotting was used to assess DMBT1 knockdown following siRNA transfection (n = 3/group). (B) HUVEC proliferation was assessed via MTT assay following treatment with MSC^N-Exos, MSCs^Con-Exos, and MSC^{DMBT1 RNAi}-Exos (n = 3/group). *P < 0.05, *** P < 0.001. (C) Western blotting was used to assess DMBT1, p-Akt, β-catenin, and VEGF expression levels in HUVECs in different treatment groups. (D) Cell cycle analyses revealed that HUVECs treated with MSCs^Con-Exos exhibited a higher frequency of cells in S phase as compared with HUVECs treated with MSC^{DMBT1 siRNA}-Exos (43.22% vs 16.04%). (E) HUVEC migration following treatment with MSC^N-Exos, MSC^Con-Exos, or MSC^{DMBT1 RNAi}-Exos was assessed via wound healing assay (n = 3/group). (F) Migration rates were quantified (n = 3/group). **P < 0.05. DMBT1, deleted in malignant brain tumors 1; siRNA, small interfering RNA; HUVEC: human umbilical vein endothelial cell; VEGF, vascular endothelial growth factor; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; PE-A: phycoerythrin absorbance.