Evidence map›Paper›PMID 33815127›Full record

ArticleFrontiers in physiology2020

Transcriptome Analysis Reveals Downregulation of Urocortin Expression in the Hypothalamo-Neurohypophysial System of Spontaneously Hypertensive Rats.

Andrew Martin, Andre S Mecawi, Vagner R Antunes, Song T Yao, Jose Antunes-Rodrigues, Julian F R Paton, Alex Paterson, Michael Greenwood, Olivera Šarenac, Bojana Savić and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 6 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

13 authors at 6 institutions in 6 countries.

Andrew MartinBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom.
Andre S MecawiLaboratory of Neuroendocrinology, Department of Biophysics, Paulista School of Medicine, Federal University of São Paulo, São Paulo, Brazil.
Vagner R AntunesBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom.
Song T YaoBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom.
Jose Antunes-RodriguesDepartment of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
Julian F R PatonManaaki Mānawa, The Heart Research Centre, University of Auckland, Auckland, New Zealand.
Alex PatersonBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom.
Michael GreenwoodBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom.
Olivera ŠarenacBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom.
Bojana SavićFaculty of Medicine, Institute of Pharmacology, Clinical Pharmacology and Toxicology, University of Belgrade, Belgrade, Serbia.
Nina Japundžić-ŽigonFaculty of Medicine, Institute of Pharmacology, Clinical Pharmacology and Toxicology, University of Belgrade, Belgrade, Serbia.
David MurphyBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom.
Charles C T HindmarchBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, United Kingdom.
University of Bristol · GBUniversity of Belgrade · RSQueen's University · CAUniversidade de São Paulo · BRUniversidade Federal de São Paulo · BRUniversity of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The chronically increased blood pressure characteristic of essential hypertension represents an insidious and cumulative risk for cardiovascular disease. Essential hypertension is a multifactorial condition, with no known specific aetiology but a strong genetic component. The Spontaneously Hypertensive rat (SHR) shares many characteristics of human essential hypertension, and as such is a commonly used experimental model. The mammalian hypothalamo-neurohypophyseal system (HNS) plays a pivotal role in the regulation of blood pressure, volume and osmolality. In order to better understand the possible role of the HNS in hypertension, we have used microarray analysis to reveal differential regulation of genes in the HNS of the SHR compared to a control normotensive strain, the Wistar Kyoto rat (WKY). These results were validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). One of the genes identified and validated as being downregulated in SHR compared to WKY was that encoding the neuropeptide urocortin (Ucn). Immunohistochemical analyses revealed Ucn to be highly expressed within magnocellular neurons of the PVN and SON, with pronounced localisation in dendritic projections containing oxytocin and vasopressin. When Ucn was overexpressed in the PVN of the SHR by

Indexed as

hypertensionhypothalamo-neurohypophyseal systemmicroarraySHRspectral analysistranscriptomeUCN

Identifiers

PMID33815127
PMCPMC8011454
OpenAlexW3122048926

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.