Research Article

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

Figure 1

Disease-specific miR-101-3p expression and the effect of cigarette smoke extract (CSE) on ASMC. (a) Disease-specific miR-101-3p gene expressions in unstimulated ASMC from healthy nonsmokers (n = 6), active non-COPD smokers (n = 6), and COPD patients (n = 8). Bars represent the mean ± S.E.M. of the corresponding patient group. (b) Gene expression of miR-101-3p in ASMC exposed for 24 hours to dilutions of CSE. Bars represent the mean ± S.E.M. of independent experiments in three cell lines of each tissue donor group. miR-101-3p expression was compared to untreated (control) ASMC in each group. (c) Z-stack projection photos acquired by confocal microscopy (Nikon, 60x magnification) of fragmented mitochondria morphology after 24 hours of exposure to CSE. Mitochondria are indicated by cytochrome c (green) staining. Similar results were obtained in three additional experiments.
(a)
(b)
(c)