ArticleThe Journal of biological chemistry2017
A repressive role of enhancer of zeste homolog 2 in 11β-hydroxysteroid dehydrogenase type 2 expression in the human placenta.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Prenatal glucocorticoids exposure and adverse cardiovascular effects in offspring.Frontiers in endocrinology · 2024Review
- Role of EZH2-mediated H3K27me3 in placental ADAM12-S expression: implications for fetoplacental growth.BMC medicine · 2022Article
- The low-expression programming of 11β-HSD2 mediates osteoporosis susceptibility induced by prenatal caffeine exposure in male offspring rats.British journal of pharmacology · 2020Article
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- Cortisol Regeneration in the Fetal Membranes, A Coincidental or Requisite Event in Human Parturition?Frontiers in physiology · 2020Review
- The Attenuation of Trophoblast Invasion Caused by the Downregulation of EZH2 Is Involved in the Pathogenesis of Human Recurrent Miscarriage.Molecular therapy. Nucleic acids · 2019Article
- Mechanisms for establishment of the placental glucocorticoid barrier, a guard for life.Cellular and molecular life sciences : CMLS · 2019Review
- EZH2 Inhibition Ameliorates Transverse Aortic Constriction-Induced Pulmonary Arterial Hypertension in Mice.Canadian respiratory journal · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which acts as a placental glucocorticoid barrier, is silenced in cytotrophoblasts but substantially up-regulated during syncytialization. However, the repressive mechanism of 11β-HSD2 expression before syncytialization and how this repression is lifted during syncytialization remain mostly unresolved. Here we found that enhancer of zeste homolog 2 (EZH2) accounts for the silence of 11β-HSD2 expression via trimethylation of histone H3 lysine 27 at the promoter of the 11β-HSD2 gene. Further studies revealed that, upon syncytialization, human chorionic gonadotropin reduced the phosphorylation of retinoblastoma protein (pRB) via activation of the cAMP/PKA pathway, which sequesters E2F transcription factor 1 (E2F1), the transcription factor for EZH2 expression. As a result of inactivation of the pRB-E2F1-EZH2 pathway, the repressive marker trimethylation of histone H3 lysine 27 at the 11β-HSD2 promoter is removed, which leads to the robust expression of 11β-HSD2 during syncytialization.
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Registered trials
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