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Fig. 2 | Cell & Bioscience

Fig. 2

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

Fig. 2

Hypoxic mitochondrial dysfunction in PASMCs is mediated by AIF. A Activity of complexes I, II and V after pretreatment with AIF overexpressed plasmid (n = 5–6). B Representative images and averaged values of mitochondrial ROS (n = 6). Scale bars: 50 μm. C The oxygen consumption rates of cultured rat PASMCs, maximal respiration, spare respiratory capacity and derived mitochondrial ATP production were calculated following oligomycin and FCCP treatment (n = 3). D Glycolysis and glycolytic reserve following treatment with 10 mM glucose and 1 μM oligomycin were measured in cultured PASMCs, and nonglycolytic acidification after treatment with 100 mM 2-deoxyglucose was detected (n = 3). E Western blot analysis of HK II, PKM2 and PDH protein expression in PASMCs in the presence or absence of hypoxia (n = 6–8). 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

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