Evidence map›Paper›PMID 24801305›Full record

ArticleThe Journal of physiology2014

Mid- to late term hypoxia in the mouse alters placental morphology, glucocorticoid regulatory pathways and nutrient transporters in a sex-specific manner.

J S M Cuffe, S L Walton, R R Singh, J G Spiers, H Bielefeldt-Ohmann, L Wilkinson, M H Little, K M Moritz

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PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
18.7field-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

69 citing papers in PubMed, 134 citations in OpenAlex.

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  19. The Placenta's Role in Sexually Dimorphic Fetal Growth Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2022
    Review
  20. Article

9 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

J S M CuffeSchool of Biomedical Sciences, The University of Queensland, St Lucia, Queensland, Australia.
S L WaltonSchool of Biomedical Sciences, The University of Queensland, St Lucia, Queensland, Australia.
R R SinghSchool of Biomedical Sciences, The University of Queensland, St Lucia, Queensland, Australia.
J G SpiersSchool of Biomedical Sciences, The University of Queensland, St Lucia, Queensland, Australia.
H Bielefeldt-OhmannSchool of Veterinary Science, The University of Queensland, Gatton, Queensland, Australia.
L WilkinsonInstitute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland, Australia.
M H LittleInstitute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland, Australia.
K M MoritzSchool of Biomedical Sciences, The University of Queensland, St Lucia, Queensland, Australia k.moritz@uq.edu.au.
University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maternal hypoxia is a common perturbation that can disrupt placental and thus fetal development, contributing to neonatal impairments. Recently, evidence has suggested that physiological outcomes are dependent upon the sex of the fetus, with males more susceptible to hypoxic insults than females. This study investigated the effects of maternal hypoxia during mid- to late gestation on fetal growth and placental development and determined if responses were sex specific. CD1 mice were housed under 21% or 12% oxygen from embryonic day (E) 14.5 until tissue collection at E18.5. Fetuses and placentas were weighed before collection for gene and protein expression and morphological analysis. Hypoxia reduced fetal weight in both sexes at E18.5 by 7% but did not affect placental weight. Hypoxia reduced placental mRNA levels of the mineralocorticoid and glucocorticoid receptors and reduced the gene and protein expression of the glucocorticoid metabolizing enzyme HSD11B2. However, placentas of female fetuses responded differently to maternal hypoxia than did placentas of male fetuses. Notably, morphology was significantly altered in placentas from hypoxic female fetuses, with a reduction in placental labyrinth blood spaces. In addition mRNA expression of Glut1, Igf2 and Igf1r were reduced in placentas of female fetuses only. In summary, maternal hypoxia altered placental formation in a sex specific manner through mechanisms involving placental vascular development, growth factor and nutrient transporter expression and placental glucocorticoid signalling. This study provides insight into how sex differences in offspring disease development may be due to sex specific placental adaptations to maternal insults.

Indexed as

11-beta-Hydroxysteroid Dehydrogenase Type 2Amino Acid Transport System AAnimalsBlood GlucoseCorticosteroneFemaleGlucose Transporter Type 1HypoxiaInsulin-Like Growth Factor IIMaleMicePlacentaPlacentationPregnancyReceptor, IGF Type 1RNA, Messenger11-beta-Hydroxysteroid Dehydrogenase Type 2Amino Acid Transport System ABlood GlucoseCorticosteroneGlucose Transporter Type 1IGF2 protein, mouseInsulin-Like Growth Factor IIReceptor, IGF Type 1RNA, MessengerSlc2a1 protein, mouseSlc38a1 protein, mouse

Identifiers

PMID24801305
PMCPMC4214664
OpenAlexW2138636041

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.