Evidence map›Paper›PMID 26039155›Full record

ArticleEndocrinology2015

Maternal Dexamethasone Treatment Alters Tissue and Circulating Components of the Renin-Angiotensin System in the Pregnant Ewe and Fetus.

Alison J Forhead, Juanita K Jellyman, Miles J De Blasio, Emma Johnson, Dino A Giussani, Fiona Broughton Pipkin, Abigail L Fowden

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

8 citing papers in PubMed, 14 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

7 authors at 2 institutions in 1 country.

Alison J ForheadDepartment of Physiology, Development and Neuroscience (A.J.F., J.K.J., M.J.D.B., E.J., D.A.G., A.L.F.), University of Cambridge, Cambridge CB2 3EG, United Kingdom; Department of Biological and Medical Sciences (A.J.F.), Oxford Brookes University, Oxford OX3 0BP, United Kingdom; and Department of Obstetrics and Gynaecology (F.B.P.), University of Nottingham, Nottingham NG5 1PB, United Kingdom.
Juanita K JellymanDepartment of Physiology, Development and Neuroscience (A.J.F., J.K.J., M.J.D.B., E.J., D.A.G., A.L.F.), University of Cambridge, Cambridge CB2 3EG, United Kingdom; Department of Biological and Medical Sciences (A.J.F.), Oxford Brookes University, Oxford OX3 0BP, United Kingdom; and Department of Obstetrics and Gynaecology (F.B.P.), University of Nottingham, Nottingham NG5 1PB, United Kingdom.
Miles J De BlasioDepartment of Physiology, Development and Neuroscience (A.J.F., J.K.J., M.J.D.B., E.J., D.A.G., A.L.F.), University of Cambridge, Cambridge CB2 3EG, United Kingdom; Department of Biological and Medical Sciences (A.J.F.), Oxford Brookes University, Oxford OX3 0BP, United Kingdom; and Department of Obstetrics and Gynaecology (F.B.P.), University of Nottingham, Nottingham NG5 1PB, United Kingdom.
Emma JohnsonDepartment of Physiology, Development and Neuroscience (A.J.F., J.K.J., M.J.D.B., E.J., D.A.G., A.L.F.), University of Cambridge, Cambridge CB2 3EG, United Kingdom; Department of Biological and Medical Sciences (A.J.F.), Oxford Brookes University, Oxford OX3 0BP, United Kingdom; and Department of Obstetrics and Gynaecology (F.B.P.), University of Nottingham, Nottingham NG5 1PB, United Kingdom.
Dino A GiussaniDepartment of Physiology, Development and Neuroscience (A.J.F., J.K.J., M.J.D.B., E.J., D.A.G., A.L.F.), University of Cambridge, Cambridge CB2 3EG, United Kingdom; Department of Biological and Medical Sciences (A.J.F.), Oxford Brookes University, Oxford OX3 0BP, United Kingdom; and Department of Obstetrics and Gynaecology (F.B.P.), University of Nottingham, Nottingham NG5 1PB, United Kingdom.
Fiona Broughton PipkinDepartment of Physiology, Development and Neuroscience (A.J.F., J.K.J., M.J.D.B., E.J., D.A.G., A.L.F.), University of Cambridge, Cambridge CB2 3EG, United Kingdom; Department of Biological and Medical Sciences (A.J.F.), Oxford Brookes University, Oxford OX3 0BP, United Kingdom; and Department of Obstetrics and Gynaecology (F.B.P.), University of Nottingham, Nottingham NG5 1PB, United Kingdom.
Abigail L FowdenDepartment of Physiology, Development and Neuroscience (A.J.F., J.K.J., M.J.D.B., E.J., D.A.G., A.L.F.), University of Cambridge, Cambridge CB2 3EG, United Kingdom; Department of Biological and Medical Sciences (A.J.F.), Oxford Brookes University, Oxford OX3 0BP, United Kingdom; and Department of Obstetrics and Gynaecology (F.B.P.), University of Nottingham, Nottingham NG5 1PB, United Kingdom.
University of Cambridge · GBOxford Brookes University · GB

Funding

Biotechnology and Biological Sciences Research Council BB/E002668/1Biotechnology and Biological Sciences Research Council BB/H01697X/1British Heart Foundation RG/06/006/22028British Heart Foundation RG/11/16/29260
6 · The paper itself

Abstract

Antenatal synthetic glucocorticoids promote fetal maturation in pregnant women at risk of preterm delivery and their mechanism of action may involve other endocrine systems. This study investigated the effect of maternal dexamethasone treatment, at clinically relevant doses, on components of the renin-angiotensin system (RAS) in the pregnant ewe and fetus. From 125 days of gestation (term, 145 ± 2 d), 10 ewes carrying single fetuses of mixed sex (3 female, 7 male) were injected twice im, at 10-11 pm, with dexamethasone (2 × 12 mg, n = 5) or saline (n = 5) at 24-hour intervals. At 10 hours after the second injection, maternal dexamethasone treatment increased angiotensin-converting enzyme (ACE) mRNA levels in the fetal lungs, kidneys, and heart and ACE concentration in the circulation and lungs, but not kidneys, of the fetuses. Fetal cardiac mRNA abundance of angiotensin II (AII) type 2 receptor decreased after maternal dexamethasone treatment. Between the two groups of fetuses, there were no significant differences in plasma angiotensinogen or renin concentrations; in transcript levels of renal renin, or AII type 1 or 2 receptors in the lungs and kidneys; or in pulmonary, renal or cardiac protein content of the AII receptors. In the pregnant ewes, dexamethasone administration increased pulmonary ACE and plasma angiotensinogen, and decreased plasma renin, concentrations. Some of the effects of dexamethasone treatment on the maternal and fetal RAS were associated with altered insulin and thyroid hormone activity. Changes in the local and circulating RAS induced by dexamethasone exposure in utero may contribute to the maturational and tissue-specific actions of antenatal glucocorticoid treatment.

Indexed as

Maternal ExposureAngiotensinogenAnimalsDexamethasoneFemaleFetal DevelopmentFetusMalePeptidyl-Dipeptidase APregnancyReceptors, AngiotensinReninRenin-Angiotensin SystemSheepAngiotensinogenDexamethasonePeptidyl-Dipeptidase AReceptors, AngiotensinRenin

Identifiers

PMID26039155
PMCPMC4511127
OpenAlexW2188028366

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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.