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. 2017 Jul 26;7:6618. doi: 10.1038/s41598-017-07011-3

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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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FTI-277 prevented burn-induced impaired mitochondrial respiratory supercomplex assembly in skeletal muscle. At 3 days after burn or sham-burn, respiratory supercomplexes in the mitochondria in skeletal muscle were separated by blue native (BN) PAGE followed by second-dimensional SDS-PAGE and visualized using antibodies for NDFUA9 (a component of complex I), and UQCRC2 and RISP (components of complex III). The percentage of the complex I-containing largest supercomplex (SC) signal intensity was decreased in vehicle-treated burned mice compared with sham-burned mice. FTI-277 treatment inhibited the burn-induced alteration in the supercomplexes. On the other hand, total protein abundance of UQCRC2 was not altered by burn injury or FTI-277 (E). SDHA (a component of complex II) was used as a control. WB: Western blotting.