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. 2022 Jan 10;13:4. doi: 10.1186/s13287-021-02677-z

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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. 2 — Contribution of Cav3.2 T-type calcium channel to MSC-H cell migration. Rhod-3 probes emitted red fluorescence when reacting with intercellular free calcium. MSC-H cells displayed higher fluorescent intensity than MSC-C cells, suggesting a significant increase of intercellular free calcium in MSC-H cells. But the fluorescence was substantially abrogated by either blockage of Cav3.2 T-type calcium channel with 8 μmol/l ABT-639 or HMGB1 knock-down as shown in siH2 and siH3 cells (a). In transwell assay, the population of migrated cells was increased in MSC-H cells when compared to MSC-C cells but diminished with increasing doses of ABT-639 (b). MSC-H cells showed a significant increase of cytoplasmic HMGB1. Knock-down of HMGB1 markedly reduced cytoplasmic HMGB1 level as shown in siH2 and siH3 cells. The siH1 cells had little change of cytoplasmic HMGB1 expression and therefore was excluded from further studies. The expression of Cav3.2 T-type calcium channel encoded by CACNA1H was increased 1.5-fold in MSC-H cells but inhibited by HMGB1 knock-down as shown in siH2 and siH3 cells (c)