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. 2019 Aug 15;9:11929. doi: 10.1038/s41598-019-47457-1

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© The Author(s) 2019

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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Overexpression of PGC-1α partially rescues 3-oxo-C12-HSL-induced impairment in mitochondrial biogenesis and cellular respiration. BEAS-2B cells were transduced with adenovirus (MOI 25) expressing GFP (AdGFP) or PGC-1α (AdPGC-1α) for 48 hours (A,B) or 72 hours (C–H) prior to treatment with 100 μM 3-oxo-C12-HSL. QPCR for PGC-1α (A) and TFAM (B) and western blot representative of three independent experiments for PGC-1α and TFAM (C) confirms that PGC-1α overexpression prevents the attenuation in the expression of PGC-1α and TFAM caused by 3-oxo-C12-HSL. Full length blots are presented in Supplementary Fig. 3D–H. Seahorse XF Mito Stress Test analysis demonstrates that in cells treated with 3-oxo-C12-HSL, PGC-1α overexpression significantly increased basal respiration (E) maximal respiration (F) spare respiratory capacity, and ATP-linked respiration (G). Results are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 by one-way ANOVA with Tukey’s multiple comparisons test, n = 4 (A–C) or 6 (D–G) independent experiments.