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Fig. 7 | Cell & Bioscience

Fig. 7

From: Ubiquitinated AIF is a major mediator of hypoxia-induced mitochondrial dysfunction and pulmonary artery smooth muscle cell proliferation

Fig. 7

UBA52/AIF axis is responsible for increased cell autophagy and proliferation in response to hypoxia treatment. A Mitochondrial ROS was visualized by the mitochondrially targeted superoxide indicator (MitoSOX). Treatment with UBA52 siRNA blocked the increase in MitoSOX under hypoxia, whereas UBA52 plus AIF siRNA reversed this effect (n = 6). Scale bars: 50 μm. B Representative autophagic flux monitored by eGFP-mRFP LC3 plasmid transfection. The formation of autophagosomes was calculated (n = 6). Scale bars: 50 μm. C Western blot analysis of LC3BII and Pink in PASMCs cotransfected with UBA52 and AIF siRNA (n = 5). D, E CCK8 and 5-ethynyl-2-deoxyuridine (EdU) assays were used to determine the effects of UBA52 and AIF on cell proliferation (n = 6). F The number of cells in each phase of the cell cycle was examined by flow cytometry (n = 3). All data are presented as the means ± standard deviation. *p < 0.05; **p < 0.01; ***p < 0.001; Nor normoxia, Hyp hypoxia, NC negative control, si small interfering RNA

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