Epigenetic regulation of the placental HSD11B2 barrier and its role as a critical regulator of fetal development

Togher, Katie L.; O’Keeffe, Majella; Khashan, Ali S.; Gutiérrez, Humberto; Kenny, Louise C.; O’Keeffe, Gerard W.

doi:10.4161/epi.28703

Cited by 80 publications

(86 citation statements)

References 76 publications

(103 reference statements)

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“…This progressive increase in HSD11B2 expression with advancing pregnancy has been demonstrated in the human [20,24,25] and baboon [26] placenta previously. Conversely, HSD11B2 mRNA is abundantly expressed in the labyrinth zone and extra embryonic membranes of the mouse placenta until E15.5 but then halts at E16.5 [27].…”

Section: Discussionmentioning

confidence: 84%

“…To determine if maternal exposure to LPS altered the expression of placental HSD11B2, which is a critical regulator of fetal development [20], we next examined the expression of placental HSD11B2 using real-time PCR and immunocytochemistry at each of these time points. HSD11B2 protein (Fig.…”

Section: The Effects Of Maternal Lps On Placental Cytokine and Hsd11bmentioning

confidence: 99%

“…As cortisol/corticosterone levels are known to regulate HSD11B2 expression [20], we next examined maternal corticosterone levels at E18 in pregnant dams that received I.P LPS or saline on E16. We found that maternal corticosterone levels were significantly lower in the LPS group compared to saline treated controls using an ELISA on maternal plasma samples (Fig.…”

Section: The Effects Of Maternal Lps On Placental Cytokine and Hsd11bmentioning

confidence: 99%

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LPS alters placental inflammatory and endocrine mediators and inhibits fetal neurite growth in affected offspring during late gestation

et al. 2014

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Section: Discussionmentioning

confidence: 84%

Section: The Effects Of Maternal Lps On Placental Cytokine and Hsd11bmentioning

confidence: 99%

Section: The Effects Of Maternal Lps On Placental Cytokine and Hsd11bmentioning

confidence: 99%

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LPS alters placental inflammatory and endocrine mediators and inhibits fetal neurite growth in affected offspring during late gestation

et al. 2014

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“…ACTH stimulates secretion of cortisol from the adrenal glands. Circulating cortisol provides negative feedback by activating GR and mineralocorticoid receptor (MR) in the hippocampus and GR in the hypothalamus and anterior pituitary gland to maintain homeostasis 2,3,34 .…”

Section: Gc Metabolism and Signaling In Pregnancymentioning

confidence: 99%

Effects of antenatal glucocorticoids on the developing brain

et al. 2016

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Glucocorticoids (GCs) regulate distinct physiological processes in the developing fetus, in particular accelerating organ maturation that enables the fetus to survive outside the womb. In preterm birth, the developing fetus does not receive sufficient exposure to endogenous GCs in utero for proper organ development predisposing the neonate to complications including intraventricular hemorrhage, respiratory distress syndrome (RDS) and necrotizing enterocolitis (NEC). Synthetic GCs (sGCs) have proven useful in the prevention of these complications since they are able to promote the rapid maturation of underdeveloped organs present in the fetus. While these drugs have proven to be clinically effective in the prevention of IVH, RDS and NEC, they may also trigger adverse developmental side effects. This review will examine the current clinical use of antenatal sGC therapy in preterm birth, their placental metabolism, and their effects on the developing brain.

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“…Animal stress models revealed that the timing of the maternal stressor during gestation is a key factor for the offspring to be born SGA or LGA [48]. Furthermore, placental development and function, especially an impairment of the placental barrier which normally limits fetal exposure to maternal stress hormones, is thought to play a central role in the severity of maternal stress effects [49,50]. Taken together, both over and undernutrition are associated with developmental programming.…”

Section: Overnutritionmentioning

confidence: 99%

Developmental Origins of Disease - Crisis Precipitates Change

Reichetzeder

Putra

et al. 2016

Cell Physiol Biochem

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The concept of developmental origins of diseases has gained a huge interest in recent years and is a constantly emerging scientific field. First observations hereof originated from epidemiological studies, linking impaired birth outcomes to adult chronic, noncommunicable disease. By now there is a considerable amount of both epidemiological and experimental evidence highlighting the impact of early life events on later life disease susceptibility. Albeit far from being completely understood, more recent studies managed to elucidate underlying mechanisms, with epigenetics having become almost synonymous with developmental programming. The aim of this review was to give a comprehensive overview of various aspects and mechanisms of developmental origins of diseases. Starting from initial research foci mainly centered on a nutritionally impaired intrauterine environment, more recent findings such as postnatal nutrition, preterm birth, paternal programming and putative interventional approaches are summarized. The review outlines general underlying mechanisms and particularly discusses mechanistic explanations for sexual dimorphism in developmental programming. Furthermore, novel hypotheses are presented emphasizing a non-mendelian impact of parental genes on the offspring's phenotype.

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Epigenetic regulation of the placental HSD11B2 barrier and its role as a critical regulator of fetal development

Cited by 80 publications

References 76 publications

LPS alters placental inflammatory and endocrine mediators and inhibits fetal neurite growth in affected offspring during late gestation

LPS alters placental inflammatory and endocrine mediators and inhibits fetal neurite growth in affected offspring during late gestation

Effects of antenatal glucocorticoids on the developing brain

Developmental Origins of Disease - Crisis Precipitates Change

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