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. 2022 Jan 26;18(3):1113–1126. doi: 10.1007/s12015-021-10261-4

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© The Author(s) 2021

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/.

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Fig. 6 — The human ASC-EVs and mouse MSC-EVs affect the expression of CD36 and CD206 of BV-2 cells after Aβ stimulation. EVs from the human ASC and mouse MSC supernatants were isolated via differential (ultra)-centrifugation. Resting BV-2 cells were primed for 3 h with 1 µg/ml LPS before stimulation with 10 µM of Aβ aggregates in the presence and absence of 6.5 × 10⁴ ± 1.5 × 10⁴ EVs/cell (NTA quantification). After 24 h of stimulation surface expressions of (A) CD36 and (B) CD206 on BV-2 cells were evaluated by flow cytometry. Data represent means ± SEM (n = 3). Statistics were calculated with the Mann Whitney U-Test