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. 2022 Oct 4;13:491. doi: 10.1186/s13287-022-03178-3

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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 — PI3K-AKT signaling is required for the increase of HKII activity. a The protein level of HKII is not changed upon TNFα and IFNγ stimulation. b HKII activity is increased quickly after TNFα and IFNγ stimulated. c MSCs were pretreated with LY294002 (LY) or triciribine (TCN) for 1 h and then TNFα and IFNγ were added into the medium for 1 h. HKII activity of MSCs was analyzed by hexokinase activity assay. d MSCs were infected by adenovirus expressing constitutive active form Myr-AKT or dominant-negative AKT (DN-AKT) two days before TNFα and IFNγ stimulation. After TNFα and IFNγ treatment for 1 h, HKII activity of MSCs was analyzed by hexokinase activity assay. Data are presented as mean ± SEM. of triplicates (b–d) ***, p < 0.001