Pre-eclampsia: a disorder of placental mitochondria?

Widschwendter, Martin; Schröcksnadel, H.; Mörtl, M

doi:10.1016/s1357-4310(98)01293-3

Cited by 50 publications

(29 citation statements)

References 38 publications

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“…Morphological and proteomic studies suggest mitochondrial involvement in PE [37,38]. Indeed, defects in mitochondria might be a possible cause of PE [39]. The mitochondrial transport chain is the primary source of reactive oxygen species (ROS) [40] and its energy metabolism increases with SIRT3 activation, resulting in inhibition of apoptosis [35].…”

Section: Discussionmentioning

confidence: 99%

Protective proteins and telomere length in placentas from patients with pre-eclampsia in the last trimester of gestation

et al. 2017

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Introduction Visfatin/nicotinamide phosphoribosyltransferase (Nampt), an enzyme involved in energy metabolism and sirtuins, SIRT1 and SIRT3, which are NAD-dependent deacetylases, are critical for cellular function. All three either regulate or are regulated by intracellular NAD+ levels and therefore available cellular energy, important for placental cell survival and successful pregnancy. This study investigates whether these protective proteins are involved in the placental pathophysiology of pre-eclampsia (PE) and if they are associated with 8-oxo-deoxyguanosine (8OHdG), a marker of oxidative damage or with placental telomere length. Methods Maternal blood and placental samples were collected from 31 patients with PE and 30 controls between 31 and 40 weeks gestation. Quantitative immunohistochemistry was performed on placental specimens for visfatin/Nampt, SIRT1, SIRT3, and nuclear 8OHdG. Plasma visfatin was measured by ELISA and telomere length by Southern blot analysis of telomere restriction fragments. Results Visfatin/Nampt and SIRT1 in syncytiotrophoblast decreased in PE compared to controls (p < 0.0001, p = 0.004 respectively). SIRT3 decreased in PE most significantly at preterm (p = 0.002). 8OHdG was only significantly lower in preterm controls compared to term controls (p = 0.01) and correlated with SIRT1 in all samples (r = 0.27). Telomere length was not different in PE and controls. Discussion Decreased visfatin/Nampt, SIRT1 and SIRT3 in syncytiotrophoblast in PE suggests a lack of placental reserve in metabolic energy efficiency, increased inflammation, and lower resistance to environmental stressors. However, there was little effect on nuclear function, or evidence of genomic DNA damage, which would lead to cellular senescence and death.

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Section: Discussionmentioning

confidence: 99%

Protective proteins and telomere length in placentas from patients with pre-eclampsia in the last trimester of gestation

et al. 2017

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“…The increasing metabolic activity of placental mitochondria throughout gestation results in excessive production of reactive oxygen species (ROS) and oxidative stress [4–5], which becomes exaggerated in pregnancies complicated by preeclampsia [6–7], IUGR [8–9], gestational diabetes[10] and maternal obesity [11–12]. Several lines of evidence indicate that placental mitochondrial dysfunction is central to these pathological conditions [13–14]. In addition to being a major site for ROS production, mitochondria also become a target for ROS-induced damage and can be severely compromised by prolonged oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Measurement of mitochondrial respiration in trophoblast culture

Maloyan¹,

Mele²,

Muralimanohara³

et al. 2012

Placenta

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Pregnancy is a state of oxidative stress, which becomes exaggerated under pathological conditions, such as preeclampsia, IUGR, diabetes and obesity, where placental mitochondrial dysfunction is observed. The majority of investigations utilize isolated mitochondria when measuring mitochondrial activity in placenta. However, this does not provide a complete physiological readout of mitochondrial function. This technical note describes a method to measure respiratory function in intact primary syncytiotrophoblast from human term placenta.

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“…Die Spekulationen reichen von einer fehlerhaften lokalen Modulation der Immunabwehr mit der daraus erklärbaren Inaktivierung des Invasionspotentials der Trophoblasten [13,14] bis zu einem initialen Defekt in den trophoblastären Mitochondrien [15] (Abb. 1).…”

Section: Derzeitiges Konzept Der Pathogeneseunclassified

Prädiktion der Präeklampsie: neue Hypothesen, neue Ansätze

Müller

Widschwendter²,

Mörtl³

et al. 1998

Gynäkol Geburtshilfliche Rundsch

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Die Präeklampsie ist eine Multiorganerkrankung, die bei 5,8% aller Erstgebärenden auftritt. Die Krankheit zeigt einen progressiven Verlauf mit sehr unterschiedlichen Symptomen und einer variablen Progressionsrate. Hypertonie und schwangerschaftsinduzierte Proteinurie sind die klassischen Manifestationen. Die Krankheit verursacht schwere Komplikationen bei Mutter und Fetus. Es gibt weder Prädiktionsfaktoren noch Präventions- und Therapiestrategien. Die bisherigen Ergebnisse deuten entschieden darauf hin, dass ein gänzliches Ausbleiben oder eine nur unvollständige Invasion von Trophoblastzellen (Ende des 1., Beginn des 2. Trimenons) in die Spiralarterien, was deren Verengung und Schäden am Endothelium zur Folge hat, für das Auftreten dieser Krankheit (3. Trimenon) verantwortlich ist. Der Gund für diese gestörte trophoblastäre Invasion ist unbekannt. Die therapeutischen Möglichkeiten beschränken sich darauf, die aufgetretenen klinischen Symptome zu behandeln. In dieser Arbeit diskutieren wir die Möglichkeiten, um spezifische und sensitive prädiktive Parameter entsprechend dem heutigen Wissen über die Pathophysiologie dieser schwangerschaftsinduzierten schweren Erkrankung zu finden.

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Pre-eclampsia: a disorder of placental mitochondria?

Cited by 50 publications

References 38 publications

Protective proteins and telomere length in placentas from patients with pre-eclampsia in the last trimester of gestation

Protective proteins and telomere length in placentas from patients with pre-eclampsia in the last trimester of gestation

Measurement of mitochondrial respiration in trophoblast culture

Prädiktion der Präeklampsie: neue Hypothesen, neue Ansätze

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