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. 2022 Dec 8;23(24):15566. doi: 10.3390/ijms232415566

Figure 5.

Figure 5

Ang 1-7 attenuates Ang II-mediated mitochondrial fission and ROS generation in thoracic aortic SMCs. Representative confocal images of Mitotracker red staining (A) and their analysis using the Mitochondrial Network Analysis program (MiNA plugin; ImageJ; (B)) show smaller and more fragmented mitochondria in response to Ang II-treated thoracic aortic SMCs compared to the control group (n = 6 in each group). Quantification of Mitotracker red-staining images using MiNA showing decreased mean branch length (C), mean network branches (D), and decreased mitochondrial footprint (E) in Ang II-treated VSMCs compared to control group. Ang 1-7 treatment attenuates Ang II-induced mitochondrial fission (A–E). Representative brightfield microscopy and confocal microscopy images of DHE-stained thoracic SMCs (F), along with quantification of DHE fluorescence intensity (G), show increased cellular ROS levels in Ang II-treated VSMCs compared to the control group (n = 5 in each group). Flow cytometric analysis of MitoSOX-stained thoracic aortic SMCs (H) and quantification of MitoSOX fluorescence (I) indicate increased mitochondrial ROS levels in Ang II-treated VSMCs (n = 5 in each group). Ang 1-7 treatment mitigates Ang II-mediated increased cellular and mitochondrial ROS levels in thoracic aortic SMCs (F–I). A.U.: arbitrary unit; * p < 0.05 compared with the control group; # p < 0.05 compared with Ang II group using one-way ANOVA.