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. 2017 Jun 27;7:4283. doi: 10.1038/s41598-017-04618-4

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© The Author(s) 2017

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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Effect of CypD deletion on hypercontracture, mPTP opening and cell death after 45 min hypoxia followed by reoxygenation in isolated adult mouse cardiomyocytes. Cardiomyocytes were isolated from wild type (WT) and CypD knock-out (KO) mice, were co-loaded with calcein, CoCl₂ and propidium iodide (PI) and were subjected to 45 min hypoxia and then reoxygenated. Images were collected every min during the first 5 min of reoxygenation and then every 5 min. (a) Percentage of cells exhibiting hypercontracture at the end of hypoxia and at different reoxygenation times. (b) Time course of mPTP opening and cell death during reoxygenation. Fluorescence was normalised to 100% of the maximal values. Traces from 3 to 5 experiments were averaged.