Evidence map›Paper›PMID 26780953›Full record

ArticleBMC research notes2016

Hypoxyprobe™ reveals dynamic spatial and temporal changes in hypoxia in a mouse model of endometrial breakdown and repair.

Fiona L Cousins, Alison A Murray, Jessica P Scanlon, Philippa T K Saunders

Open access · goldAbstract read
In one paragraph

Article in BMC research notes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  14. Targeting tumor vascularization: promising strategies for vascular normalization.Journal of cancer research and clinical oncology · 2021
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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.

Fiona L CousinsMedical Research Council Centre for Inflammation Research, The University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK. Fiona.Cousins@ed.ac.uk.
Alison A MurrayMedical Research Council Centre for Reproductive Health, The University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK. Alison.Murray@ed.ac.uk.
Jessica P ScanlonMedical Research Council Centre for Inflammation Research, The University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK. s0787100@exseed.ed.ac.uk.
Philippa T K SaundersMedical Research Council Centre for Inflammation Research, The University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK. p.saunders@ed.ac.uk.
Centre for Inflammation Research · GBMRC Centre for Reproductive Health · GB

Funding

Medical Research Council G1100356Medical Research Council G1100356/1Medical Research Council MR/N024524/1
6 · The paper itself

Abstract

backgroundMenstruation is the culmination of a cascade of events, triggered by the withdrawal of progesterone at the end of the menstrual cycle. Initiation of tissue destruction and endometrial shedding causes spiral arteriole constriction in the functional layer of the endometrium. Upregulation of genes involved in angiogenesis and immune cell recruitment, two processes that are essential to successful repair and remodelling of the endometrium, both thought to be induced by reduced oxygen has been reported. Evidence for stabilisation/increased expression of the transcriptional regulator hypoxia inducible factor in the human endometrium at menses has been published. The current literature debates whether hypoxia plays an essential role during menstrual repair, therefore this study aims to delineate a role for hypoxia using a sensitive detection method (the Hypoxyprobe™) in combination with an established mouse model of endometrial breakdown and repair.

resultsUsing our mouse model of menses, during which documented breakdown and synchronous repair occurs in a 24 h timeframe, in combination with the Hypoxyprobe™ detection system, oxygen tensions within the uterus were measured. Immunostaining revealed striking spatial and temporal fluctuations in hypoxia during breakdown and showed that the epithelium is also exposed to hypoxic conditions during the repair phase. Furthermore, time-dependent changes in tissue hypoxia correlated with the regulation of mRNAs encoding for the angiogenic genes vascular endothelial growth factor and stromal derived factor (Cxcl12).

conclusionsOur findings are consistent with a role for focal hypoxia during endometrial breakdown in regulating gene expression during menses. These data have implications for treatment of endometrial pathologies such as heavy menstrual bleeding.

Indexed as

AnimalsChemokine CXCL12EndometriumFemaleGene Expression ProfilingGene Expression RegulationHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMenstruationMiceMice, Inbred C57BLModels, AnimalNeovascularization, PhysiologicProgesteroneRNA, MessengerChemokine CXCL12Cxcl12 protein, mouseHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitProgesteroneRNA, MessengerVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID26780953
PMCPMC4717617
OpenAlexW2277433209

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.