Review: Placental mitochondrial function and structure in gestational disorders

Holland, Olivia J.; Nitert, Marloes Dekker; Gallo, Linda A.; Vejzovic, Meliha; Fisher, Joshua J.; Perkins, Anthony V.

doi:10.1016/j.placenta.2016.12.012

Cited by 161 publications

(157 citation statements)

References 75 publications

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“…In rats, eIF2 signalling was also shown to be heavily involved in the regulation of placental and foetal development . Likewise, oxidative phosphorylation and mitochondrial dysfunction have been associated with a range of gestational disorders . Mitochondrial dysfunction could also indicate an impairment of the antiviral immune response .…”

Section: Discussionmentioning

confidence: 99%

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Immunological observations and transcriptomic analysis of trimester‐specific full‐term placentas from three Zika virus‐infected women

et al. 2019

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Objectives Effects of Zika virus (ZIKV) infection on placental development during pregnancy are unclear. Methods Full‐term placentas from three women, each infected with ZIKV during specific pregnancy trimesters, were harvested for anatomic, immunologic and transcriptomic analysis. Results In this study, each woman exhibited a unique immune response with raised IL‐1RA, IP‐10, EGF and RANTES expression and neutrophil numbers during the acute infection phase. Although ZIKV NS3 antigens co‐localised to placental Hofbauer cells, the placentas showed no anatomic defects. Transcriptomic analysis of samples from the placentas revealed that infection during trimester 1 caused a disparate cellular response centred on differential eIF2 signalling, mitochondrial dysfunction and oxidative phosphorylation. Despite these, the babies were delivered without any congenital anomalies. Conclusion These findings should translate to improve clinical prenatal screening procedures for virus‐infected pregnant patients.

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Section: Discussionmentioning

confidence: 99%

“…32 Likewise, oxidative phosphorylation and mitochondrial dysfunction have been associated with a range of gestational disorders. 33 Mitochondrial dysfunction could also indicate an impairment of the antiviral immune response. 34 It is known that some viruses attack the host cell mitochondrial network as a form of immune evasion.…”

Section: Discussionmentioning

confidence: 99%

Immunological observations and transcriptomic analysis of trimester‐specific full‐term placentas from three Zika virus‐infected women

et al. 2019

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“…); however, mitochondrial content in the placenta has been shown altered in a range of pathologies (Holland et al . ). Maternal glucocorticoids have been shown to reduce mitochondrial content in fetal heart tissues (Richards et al .…”

Section: Discussionmentioning

confidence: 97%

“…Cellular mitochondrial content is adaptive and can change in response to cellular damage. Skeletal muscle mitochondrial content is increased in response to exercise to enhance tissue function (Broskey et al 2014); however, mitochondrial content in the placenta has been shown altered in a range of pathologies (Holland et al 2017). Maternal glucocorticoids have been shown to reduce mitochondrial content in fetal heart tissues (Richards et al 2014), and in vitro studies have demonstrated decreased mitochondrial content in endothelial cells exposed to glucocorticoids (Gero & Szabo, 2016).…”

Section: Effects Of Corticosterone On Mitochondrial Functionmentioning

confidence: 99%

Maternal corticosterone in the mouse alters oxidative stress markers, antioxidant function and mitochondrial content in placentas of female fetuses

Bartho

Holland

Moritz

et al. 2019

The Journal of Physiology

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Key points Maternal exposure to the stress hormone corticosterone is known to programme a range of sex specific disease outcomes in offspring. Sex differences in placental adaptations are thought to mediate these processes. Placental oxidative stress is implicated in a range of pregnancy disorders but the role of placental oxidative stress in sex specific disease outcomes following prenatal corticosterone exposure is unknown. This study demonstrates that maternal corticosterone reduced placental hydrogen peroxide and 8‐hydroxy‐2′‐deoxyguanosine concentrations but increased protein carbonyl content and advanced glycation end product concentrations in placentas of female fetuses but not male fetuses. These results highlight that placentas of female fetuses respond differently to maternal corticosterone exposure, with oxidative stress a major finding in placentas of female fetuses. Abstract Maternal exposure to glucocorticoids during pregnancy increases offspring risk of developing a range of sex specific disease phenotypes. These sex specific disease outcomes are thought to be in part mediated by different placental adaptations in males and females. The placenta is a highly metabolic organ which is vulnerable to the effects of oxidative stress. In other tissues, males and females have been shown to respond differently to the pro‐oxidant effects of glucocorticoids. This study therefore used a well characterized animal model of maternal corticosterone exposure to investigate sex specific alterations in reactive oxygen species production, antioxidant concentrations and mitochondrial properties that might contribute to sex differences in placental outcomes. C57BL/6 mice were implanted with osmotic minipumps containing corticosterone (33 μg kg−1 h−1) at embryonic day (E) 12.5 and placentas collected at E14.5 for analysis. Corticosterone exposure reduced placental hydrogen peroxide (H2O2) and 8‐hydroxy‐2′‐deoxyguanosine concentrations but increased protein carbonyl content and advanced glycation end product concentrations in placentas of female fetuses but not male fetuses. This dysregulation of different markers of oxidative stress may be due to increased placental activity of thioredoxin reductase in female but not male fetuses. Corticosterone reduced placental mitochondrial content but increased protein expression of the autophagosome cargo protein p62. This study demonstrates that placentas of female fetuses respond differently to maternal corticosterone exposure and highlights an important role of reactive oxygen species, mitochondrial adaptations and antioxidant responses in glucocorticoid induced programmed disease.

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“…15,16 The mitochondria control subjects many critical cell functions, which include the production of cellular energy, adenosine triphosphate, by the coupling of OP to cell respiration. 17–19 Oxidative stress-induced damage to mitochondrial structural elements (eg, lipid membrane) alters mitochondrial gene expression and promotes a deficiency in OP, 20 which results in mitochondrial dysfunction. Hundreds of nuclear DNA genes across the chromosome regulate MB and maintain mitochondrial structure and function by regulating OP.…”

Section: Introductionmentioning

confidence: 99%

Abruptio placentae risk and genetic variations in mitochondrial biogenesis and oxidative phosphorylation: replication of a candidate gene association study

Workalemahu

Enquobahrie

Gelaye

et al. 2018

American Journal of Obstetrics and Gynecology

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In this study, we replicated previous findings and provide strong evidence for DNA variants that encode for genes that are involved in mitochondrial biogenesis and oxidative phosphorylation pathways, which confers risk for abruptio placentae. These results shed light on the mechanisms that implicate DNA variants that encode for proteins in mitochondrial function that are responsible for abruptio placentae risk. Therapeutic efforts to reduce risk of abruptio placentae can be enhanced by improved biologic understanding of maternal mitochondrial biogenesis/oxidative phosphorylation pathways and identification of women who would be at high risk for abruptio placentae.

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Review: Placental mitochondrial function and structure in gestational disorders

Abstract: 22The aetiology of many gestational disorders is still unknown. However, insufficient trans-

Cited by 161 publications

References 75 publications

Immunological observations and transcriptomic analysis of trimester‐specific full‐term placentas from three Zika virus‐infected women

Immunological observations and transcriptomic analysis of trimester‐specific full‐term placentas from three Zika virus‐infected women

Maternal corticosterone in the mouse alters oxidative stress markers, antioxidant function and mitochondrial content in placentas of female fetuses

Abruptio placentae risk and genetic variations in mitochondrial biogenesis and oxidative phosphorylation: replication of a candidate gene association study

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