Research Article

MicroRNA-101-3p Suppresses mTOR and Causes Mitochondrial Fragmentation and Cell Degeneration in COPD

Figure 2

Disease-specific effect of miR-101-3p on ASMC mitochondria. (a) Western blots of mitochondria cytochrome c oxidase subunit II (MTCO2) protein expression in commercial ASMC (healthy nonsmokers (control): n = 3; COPD: n = 3) treated with miR-101-3p mimics (controls) or inhibitors (COPD). (b) Bars represent the mean ± S.E.M. of MTCO2 expression (image analysis) of three Western blots, as shown in Figure 2(a). values present comparison to untreated cells. (c) Z-stack projection photos acquired by confocal microscopy (Nikon, 60x magnification) of fragmented mitochondria morphology in ASMC of healthy nonsmokers (control, n = 3) treated with miR-101-3p mimics, or COPD-ASMC (n = 3) treated with miR-101-3p inhibitors, over 24 hours. Mitochondria are visualized by cytochrome c (green) staining. (d) Image analysis of fragmented mitochondria as described in Figure 2(c). Bars represent mean ± S.E.M. of disease-specific effects of miR-101-3p mimics and inhibitors on MTCO2 expression (300 cells/slide).
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