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. 2018 May 3;8:6997. doi: 10.1038/s41598-018-25485-7

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© The Author(s) 2018

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Autophagy inhibition blocks CPT1C protective effects against glucose starvation. (A) p62 protein levels were analyzed by immunoblotting in EV or CPT1C-hMSCs at the indicated times after glucose depletion. (B) ATP production was evaluated after 36 h of glucose starvation in the presence (last 24 h) or absence of 100 µM chloroquine. Results are shown as mean ± SEM of 2 independent experiments performed in triplicate. (C,D) Cellular viability was measured in EV or CPT1C-hMSCs in the presence or absence of glucose for 72 h with or without the addition of chloroquine (in C) or 3-MA (in D) in the last 24 h. Results are shown as mean ± SEM of 3 or 4 independent experiments performed in sextuplet. *p < 0.05.