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. Author manuscript; available in PMC: 2018 Feb 13.
Published in final edited form as: J Proteome Res. 2016 Aug 29;15(10):3813–3826. doi: 10.1021/acs.jproteome.6b00602

Figure 5.

Figure 5

HTS-treated SAECs and decreased levels of electron transport chain complexes. Proteomics analyses were performed on SAECs by nanoUHPLC–MS/MS (A). Results confirmed Western blot data on TIGAR (B) and revealed that HTS treatment promoted the up-regulation of a wide series of membrane transporters and electron transport chain complex II components and down-regulation of enzymes involved in glutathione biosynthesis (C). In panels D and E, top pathways were down- or up-regulated upon treatment with HTS, as gleaned through GO term enrichment of >2-fold down- or up-regulated proteins with DAVID. These pathways included components of electron transport chain complexes and diseases, in which these components are altered (down, panel D), or proteasome, amino acid, and nucleoside (purine and pyrimidine) metabolism and succinate dehydrogenase complex components (up, panel E). The majority of the down-regulated proteins were part of mitochondrial electron transport chain complexes I, III, IV, and V, where the majority of the components decreased at least 2-fold (asterisks in panel F), as detailed in the panel.