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. 2018 May 9;8:7323. doi: 10.1038/s41598-018-25510-9

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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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Effect of GNE knockdown on mitochondrial dysfunction: (A) Morpho-structural analysis of mitochondria: representative TEM image showing alterations in mitochondrial morphology of GNE knockdown cells, compared to vector control cells. (B) Effect of GNE knockdown on dissipation of mitochondrial membrane potential (as measured by JC-1) using confocal microscopy, magnification 60×. Loss in mitochondrial membrane potential or depolarization is indicated by increased presence of JC-1 as monomeric form (green) and consequently leading to a decrease in the red/green fluorescence intensity ratio. (C) Histogram shows the ratio of red to green fluorescence intensity observed in GNE knockdown cell lines characterizing mitochondrial membrane potential. (D) Immunoblot analysis of cell lysates from indicated cell lines with anti-procaspase 3, β-actin was used as loading control. (E) Immunoblot analysis of cell lysates from indicated cell lines with anti-PARP antibody, GAPDH was used as loading control. The statistical significance was assessed by one-way ANOVA test. P values for * is <0.05.