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. 2022 Feb 2;13:49. doi: 10.1186/s13287-022-02724-3

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© The Author(s) 2022

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. 5 — HA reinforced the paracrine ability of UC-MSCs to further activate the PI3K-AKT pathway and promote follicle survival. a Scatter diagram showing the differentially expressed proteins between MSC-CM and HA/MSC-CM according to the 440-cytokine array. b KEGG pathway analysis showing many differentially expressed proteins related to the PI3K-AKT signaling pathway. c The levels of HGF, VEGF, SCF, and EGF were measured by ELISA in MSC-CM and HA/MSC-CM (n = 3). *P < 0.05. d Western blot showing the activation of the PI3K-AKT pathway by MSC-CM and HA/MSC-CM. e Immunostaining showing the expressions of DDX4 in the ovaries in the four groups after culturing for 8 days. Scale bars = 50 μm