Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0055194
Title: Suppression of Mitochondrial Electron Transport Chain Function in the Hypoxic Human Placenta: A Role for miRNA-210 and Protein Synthesis Inhibition
Authors: Colleoni F.
Padmanabhan N. 
Yung H.-W.
Watson E.D.
Cetin I.
Tissot van Patot M.C.
Burton G.J.
Murray A.J.
Keywords: cytochrome c oxidase
cytochrome c oxidase assembly protein 10
iron sulfur protein
messenger RNA
microRNA 210
reduced nicotinamide adenine dinucleotide dehydrogenase (ubiquinone)
unclassified drug
adult
aerobic metabolism
article
cell specificity
controlled study
disorders of mitochondrial functions
energy metabolism
female
gene expression
gene function
human
human cell
human tissue
intrauterine growth retardation
mitochondrial energy transfer
mitochondrial respiration
oxidative stress
oxygen concentration
oxygen consumption
oxygen transport
pathogenesis
placenta disorder
placental hypoxia
protein processing
protein synthesis inhibition
transcription regulation
Issue Date: 2013
Citation: Colleoni F., Padmanabhan N., Yung H.-W., Watson E.D., Cetin I., Tissot van Patot M.C., Burton G.J., Murray A.J. (2013). Suppression of Mitochondrial Electron Transport Chain Function in the Hypoxic Human Placenta: A Role for miRNA-210 and Protein Synthesis Inhibition. PLoS ONE 8 (1) : e55194. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0055194
Rights: Attribution 4.0 International
Abstract: Fetal growth is critically dependent on energy metabolism in the placenta, which drives active exchange of nutrients. Placental oxygen levels are therefore vital, and chronic hypoxia during pregnancy impairs fetal growth. Here we tested the hypothesis that placental hypoxia alters mitochondrial electron transport chain (ETS) function, and sought to identify underlying mechanisms. We cultured human placental cells under different oxygen concentrations. Mitochondrial respiration was measured, alongside levels of ETS complexes. Additionally, we studied placentas from sea-level and high-altitude pregnancies. After 4 d at 1% O2 (1.01 KPa), complex I-supported respiration was 57% and 37% lower, in trophoblast-like JEG3 cells and fibroblasts, respectively, compared with controls cultured at 21% O2 (21.24 KPa); complex IV-supported respiration was 22% and 30% lower. Correspondingly, complex I levels were 45% lower in placentas from high-altitude pregnancies than those from sea-level pregnancies. Expression of HIF-responsive microRNA-210 was increased in hypoxic fibroblasts and high-altitude placentas, whilst expression of its targets, iron-sulfur cluster scaffold (ISCU) and cytochrome c oxidase assembly protein (COX10), decreased. Moreover, protein synthesis inhibition, a feature of the high-altitude placenta, also suppressed ETS complex protein levels. Our results demonstrate that mitochondrial function is altered in hypoxic human placentas, with specific suppression of complexes I and IV compromising energy metabolism and potentially contributing to impaired fetal growth. © 2013 Colleoni et al.
Source Title: PLoS ONE
URI: https://scholarbank.nus.edu.sg/handle/10635/161346
ISSN: 19326203
DOI: 10.1371/journal.pone.0055194
Rights: Attribution 4.0 International
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