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. 2021 Oct 13;11:182. doi: 10.1186/s13578-021-00681-7

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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/. 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. 1 — CV-MSCs promote the autophagy, proliferation and invasion of trophoblasts in vitro. A Representative CCK-8 assay results for JAR, JEG-3 and HTR-8 cells are shown. Trophoblast cells were treated with CV-MSC CM under hypoxic conditions. B Representative Transwell assay results for trophoblasts are shown. The number of trophoblasts that migrated through the 8-μm Transwell membrane pores was counted to determine changes in the invasive capabilities in response to CV-MSC CM under hypoxic conditions (scale bar, 50 μm). C Transmission electron microscopy (TEM) analysis showed autophagosomes in the cytoplasm of trophoblast cells treated with CV-MSC CM under hypoxic conditions (scale bar, 1 μm). D Whole cell lysates from trophoblast cells were subjected to western blotting to analyse LC3, BECN1, p62, MMP2 and MMP9 levels. β-actin was included as a loading control. ***P < 0.001