Fig. 4: Mitochondrial complex levels and respiration are dysregulated in preeclamptic placentae. | Cell Death & Disease

Fig. 4: Mitochondrial complex levels and respiration are dysregulated in preeclamptic placentae.

From: Placental mitochondrial adaptations in preeclampsia associated with progression to term delivery

Fig. 4: Mitochondrial complex levels and respiration are dysregulated in preeclamptic placentae.

a Protein levels of mitochondrial complexes II and III were increased in preeclamptic placentae from term pregnancies compared to control placentae from term pregnancies (p = 0.0360, 0.0369, fold change 1.576, 1.413, respectively). Complex II was affected by gestation (p = 0.0125) and interaction factor (p = 0.0478), complex III was affected by gestation (p = 0.0401), and complex V (ATP synthase) was affected by gestation (p = 0.0370). There was no change in the protein level of complexes I, IV and V in placentae from term pregnancies, or all complexes in placentae from pre-term pregnancies. b Representative western blot images of mitochondrial complexes. c Citrate synthase activity was affected by gestation (p < 0.0001, fold change 0.495 pre-term compared to term pregnancies). d Oxidative phosphorylation through mitochondrial complexes I (OXPHOS I) and I + II, and non-phosphorylating LEAK respiration, were increased in term preeclamptic placentae (p = 0.0084, p = 0.0199, p = 0.0310, fold change 1.188, 1.232, 1.150, respectively). Maximum capacity of the respiratory system (ETS), oxygen consumption through complex II (CI-CII) and OXPHOS IV were not different. OXPHOS I as a proportion of maximal respiratory capacity (FCF CI) was increased in term preeclamptic placentae (p = 0.0026, fold change 1.126). Reserve capacity was reduced in term preeclamptic placenta (p = 0.0042, fold change 0.745). GAPDH = Glyceraldehyde 3-phosphate dehydrogenase. N = 6–10; *P < 0.05; **P < 0.01, ***P < 0.001

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