A Functional Fetal HSD11B2[CA]n Microsatellite Polymorphism is Associated with Maternal Serum Cortisol Concentrations in Pregnant Women

Li, Jian; Chen, You‐Peng; Zi-neng, Wang; Liu, Tie-Bin; Chen, Dan; Dong, Yijia; Hocher, Berthold

doi:10.1159/000355761

Cited by 5 publications

(1 citation statement)

References 27 publications

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“…There are reports describing the mutations in the promoter region of HSD11B2 : G-209A and G126A that resulted in the lower affinity of Sp1 and NF1 transcriptional factors and consequently in the reduced expression of HSD11B2 in salt-sensitivity patients [ 29 ]. Furthermore, a relationship between the microsatellite polymorphism [CA] (tandem repeats of CA nucleotides) in fetal intron 1 of HSD11B2 and maternal plasma F levels was indicated [ 30 ].…”

Section: How Can the Function Of 11 β -Hsd2mentioning

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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Section: How Can the Function Of 11 β -Hsd2mentioning

confidence: 99%

11β-Hydroxysteroid Dehydrogenase 2 in Preeclampsia

Kosicka

Siemiątkowska

Główka

2016

International Journal of Endocrinology

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Tandem mass spectrometry determined maternal cortisone to cortisol ratio and psychiatric morbidity during pregnancy−interaction with birth weight

Hellgren

Edvinsson

Olivier

et al. 2016

Psychoneuroendocrinology

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Maternal serum cortisol has been suggested to be influenced by psychiatric morbidity, and may also influence fetal growth. However, several studies found equal cortisol levels in depressed and healthy pregnant women. Placental 11-β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) shields the fetus from maternal cortisol by conversion to cortisone, a function that may be compromised by maternal stress. We aimed to compare the serum ratio of cortisone to cortisol, in women with and without psychiatric morbidity during pregnancy. A secondary aim was to investigate whether fetal growth, approximated by infant birth weight, was associated with the cortisone to cortisol ratio. We performed tandem mass spectrometry analysis of serum cortisol and cortisone in late pregnancy in 94 women with antenatal psychiatric morbidity and 122 controls (cohort 1). We also compared the placental gene expression of HSD11B1 and 2 in another group of 69 women with psychiatric morbidity and 47 controls (cohort 2). There were no group differences in cortisol to cortisone ratio, absolute levels of cortisone and cortisol (cohort 1), or expression of HSD11B1 or 2 (cohort 2). However, cortisone to cortisol ratio was positively associated with birth weight in women with psychiatric morbidity, also after adjustment for gestational length, fetal sex, maternal height, smoking, SSRI use, and time of blood sampling (standardized β=0.35, p<0.001), with no association in the healthy controls Thus, the maternal serum cortisone to cortisol ratio does not seem to be affected by psychiatric morbidity, but psychiatric morbidity may increase fetal exposure to cortisol or other metabolic factors influencing fetal growth.

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