Elevated glucocorticoid metabolism in placental tissue from first trimester pregnancies at increased risk of pre-eclampsia

Mukherjee, S.; James, Joanna L.; Thilaganathan, B.; Whitley, Guy; Michael, A.E.; Cartwright, Judith E.

doi:10.1016/j.placenta.2011.06.014

Cited by 12 publications

(10 citation statements)

References 31 publications

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“…[7] Similarly, another study has shown that increased glucocorticoid metabolite level in the placenta increases the risk of PE. [30] Furthermore, increased stress in PE directly leads to an increase in cortisol level in the hypothalamic-pituitary-adrenal axis. This increased cortisol level is associated with hypertension and endothelial damage.…”

Section: Discussionmentioning

confidence: 99%

Elevated expression of glucocorticoid-induced leucine zipper in placental endothelial and trophoblastic cells in preeclampsia

Arlıer

2017

EJMO

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Objectives:The objective of this study was to investigate the association between normal and preeclamptic glucocorticoid-induced leucine zipper (GILZ) levels in the placenta. Methods: Placental paraffin sections (5 μm) were obtained from gestational age-matched normal (n=9) and (PE) (n=9) pregnancies. Tissue sections were immunostained with rabbit monoclonal anti-human GILZ antibodies. Staining intensity of GILZ was evaluated with a histologic scoring (HSCORE) system. Parametric (t-test) and non-parametric tests (Mann-Whitney U) were used for statistical analysis, and a p value of <0.05 was considered significant. Results: Trophoblasts and endothelial cells were shown to be the source of GILZ release. Compared with the control, PE placental samples displayed significantly increased GILZ immunostaining HSCOREs in trophoblast cell nucleus (mean±SEM, 106.8±12.1 vs 167.9±14.9; p=0.006) and endothelial cells (95.0±8.1 vs 147.2±12.3; p=0.003). Conclusion: This study suggests that GILZ release by placental trophoblasts and endothelial cells may contribute to PE pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Elevated expression of glucocorticoid-induced leucine zipper in placental endothelial and trophoblastic cells in preeclampsia

Arlıer

2017

EJMO

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“…However, in pre-eclamptic pregnancy, placental 11β-HSD2 mRNA expression and consequent enzyme activity have been found to be significantly lower than in normotensive individuals [89,90], meaning that placental cortisol levels are increased in up to 80% of preeclamptic pregnancies [86]. These changes are detectable in the first trimester, before clinical symptoms of preeclampsia evolve [85].…”

Section: Effects Of Cortisol On the Trophoblastmentioning

confidence: 99%

“…In addition, dexamethasone has been shown to induce apoptosis and necrosis in cultured human trophoblasts [83]. Furthermore, cortisol has been shown to increase expression Given the apparent detrimental effects of cortisol on the trophoblast, and therefore later placental function, it is perhaps not surprising that excessive glucocorticoid exposure in utero has been associated with intrauterine growth restriction and prematurity [79,85,86]. Ordinarily, the placenta and foetus are protected from excessive glucocorticoid exposure by placental expression of the enzyme 11β-HSD2 that converts cortisol to its inactive metabolite, cortisone, preventing activation of both the glucocorticoid receptor and MR [87,88].…”

Section: Effects Of Cortisol On the Trophoblastmentioning

confidence: 99%

Endocrine aspects of pre-eclampsia

Currie

Carty

Connell

et al. 2015

Cardiovascular Endocrinology

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“…It suggests that initially the F metabolism is more intensive in this specific type of hypertension. Unfortunately, it has been not clarified whether the disturbances in the GC metabolism underlie the PE development or they are a response to the irregularities arising from this disease [ 27 ].…”

Section: Function Of Placental 11 β -Hsd2 Imentioning

confidence: 99%

11β-Hydroxysteroid Dehydrogenase 2 in Preeclampsia

Kosicka

Siemiątkowska

Główka

2016

International Journal of Endocrinology

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Preeclampsia is a serious medical problem affecting the mother and her child and influences their health not only during the pregnancy, but also many years after. Although preeclampsia is a subject of many research projects, the etiology of the condition remains unclear. One of the hypotheses related to the etiology of preeclampsia is the deficiency in placental 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2), the enzyme which in normal pregnancy protects the fetus from the excess of maternal cortisol. The reduced activity of the enzyme was observed in placentas from pregnancies complicated with preeclampsia. That suggests the overexposure of the developing child to maternal cortisol, which in high levels exerts proapoptotic effects and reduces fetal growth. The fetal growth restriction due to the diminished placental 11β-HSD2 function may be supported by the fact that preeclampsia is often accompanied with fetal hypotrophy. The causes of the reduced function of 11β-HSD2 in placental tissue are still discussed. This paper summarizes the phenomena that may affect the activity of the enzyme at various steps on the way from the gene to the protein.

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Elevated glucocorticoid metabolism in placental tissue from first trimester pregnancies at increased risk of pre-eclampsia

Cited by 12 publications

References 31 publications

Elevated expression of glucocorticoid-induced leucine zipper in placental endothelial and trophoblastic cells in preeclampsia

Elevated expression of glucocorticoid-induced leucine zipper in placental endothelial and trophoblastic cells in preeclampsia

Endocrine aspects of pre-eclampsia

11β-Hydroxysteroid Dehydrogenase 2 in Preeclampsia

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