Evidence map›Paper›PMID 30225585›Full record

ReviewCellular and molecular life sciences : CMLS2019

Mechanisms for establishment of the placental glucocorticoid barrier, a guard for life.

Ping Zhu, Wangsheng Wang, Rujuan Zuo, Kang Sun

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
12.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Ping ZhuCenter for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200135, People's Republic of China.
Wangsheng WangCenter for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200135, People's Republic of China.
Rujuan ZuoCenter for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200135, People's Republic of China.
Kang SunCenter for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200135, People's Republic of China. sungangrenji@hotmail.com.ORCID http://orcid.org/0000-0003-2727-141X
Shanghai Jiao Tong University · CNTongji University · CN

Funding

National Key Basic Research Projects 2014CB943302National Key R & D Program of China 2017YFC1001403National Natural Science Foundation of China 31671566National Natural Science Foundation of China 81330018
6 · The paper itself

Abstract

The fetus is shielded from the adverse effects of excessive maternal glucocorticoids by 11β-HSD2, an enzyme which is expressed in the syncytial layer of the placental villi and is capable of converting biologically active cortisol into inactive cortisone. Impairment of this placental glucocorticoid barrier is associated with fetal intrauterine growth restriction (IUGR) and development of chronic diseases in later life. Ontogeny studies show that the expression of 11β-HSD2 is initiated at a very early stage after conception and increases with gestational age but declines around term. The promoter for HSD11B2, the gene encoding 11β-HSD2, has a highly GC-rich core. However, the pattern of methylation on HSD11B2 may have already been set up in the blastocyst when the trophoblast identity is committed. Instead, hCG-initiated signals appear to be responsible for the upsurge of 11β-HSD2 expression during trophoblast syncytialization. By activating the cAMP/PKA pathway, hCG not only alters the modification of histones but also increases the expression of Sp1 which activates the transcription of HSD11B2. Adverse conditions such as stress, hypoxia and nutritional restriction can cause IUGR of the fetus. It appears that different causes of IUGR may attenuate HSD11B2 expression differentially in the placenta. While stress and nutritional restriction may reduce HSD11B2 expression by increasing its methylation, hypoxia may decrease HSD11B2 expression via alternative mechanisms rather than by methylation. Herein, we summarize the advances in the study of mechanisms underlying the establishment of the placental glucocorticoid barrier and the attenuation of this barrier by adverse conditions during pregnancy.

Indexed as

11-beta-Hydroxysteroid Dehydrogenase Type 2AnimalsDNA MethylationEpigenesis, GeneticFemaleFetal Growth RetardationFetusGene Expression RegulationGlucocorticoidsHistonesHumansHydrocortisonePlacentaPregnancyPromoter Regions, GeneticSignal Transduction11-beta-Hydroxysteroid Dehydrogenase Type 2GlucocorticoidsHistonesHydrocortisone11β-hydroxysteroid dehydrogenase 2CortisolhCGHistone and epigeneticsOntogenyPlacenta

Identifiers

PMID30225585
PMCPMC11105584
OpenAlexW2891544805

What OpenQuestion holds

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.