Fig. 8: SS-31 partially rescues mitochondrial respiration, reduces reactive oxygen species and apoptosis in tafazzin defective VSMCs. | Nature Communications

Fig. 8: SS-31 partially rescues mitochondrial respiration, reduces reactive oxygen species and apoptosis in tafazzin defective VSMCs.

From: Defective vascular smooth muscle cell tafazzin impairs mitochondrial function and promotes atherosclerosis in preclinical models

Fig. 8: SS-31 partially rescues mitochondrial respiration, reduces reactive oxygen species and apoptosis in tafazzin defective VSMCs.The alternative text for this image may have been generated using AI.

A Representative Seahorse profiles of oxygen consumption rate (OCR) in VSMCs from wild type (WT), Sm22a-Taz (Taz), and Sm22a-TazH69Q (TazH) mice after nil treatment (nil) or after treatment with scrambled peptide control (Scr) or SS31 (n = 3, 1M, 2F). B Maximal OCR after FCCP in WT/Taz/TazH VSMCs after nil treatment (nil) or after treatment with scrambled peptide control (Scr) or SS31 (SS) (n = 7, 3 male (M), 4 female (F) VSMC donors). C, D MitoSOX mean fluorescence intensity fluorescence (C) and percentage of annexin V-positive cells after tert-butyl hydrogen peroxide treatment (D) in nil, scrambled peptide control (Scr) or SS31 (SS) treated WT, Taz, TazH VSMCs (n = 6, 3 M, 3 F). arb. units = arbitrary units. E Western blot with quantification for tafazzin (Taz), complex I subunit (CI) and citrate synthase (CS) in nil, scrambled peptide control (Scr) or SS31 (SS) treated TazH VSMCs. Vinc = vinculin. Data normalised to citrate synthase for tafazzin and CI or vinculin for citrate synthase (n = 3, 2 M, 1 F). For (A–E) n = number of independent experiments, 1-way ANOVA with Bonferroni-Holm post hoc. Data are shown as mean ± SEM with multiplicity adjusted p-values. Source data are provided as a Source Data file.

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