Evidence map›Paper›PMID 21814219›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2011

Refined mapping of blood pressure quantitative trait loci using congenic strains developed from two genetically hypertensive rat models.

Sivarajan Kumarasamy, Kathirvel Gopalakrishnan, Edward J Toland, Shane Yerga-Woolwine, Phyllis Farms, Eric E Morgan, Bina Joe

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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  12. Construction of two novel reciprocal conplastic rat strains and characterization of cardiac mitochondria.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  13. Article
  14. Targeted disruption of Adamts16 gene in a rat genetic model of hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  15. Article
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 1 institution in 1 country.

Sivarajan KumarasamyPhysiological Genomics Laboratory, University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
Kathirvel Gopalakrishnan
Edward J Toland
Shane Yerga-Woolwine
Phyllis Farms
Eric E Morgan
Bina Joe
University of Toledo · US

Funding

Genetics of HypertensionR01HL020176 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI JOE, BINA · 1985 to 2017
$8.1M
Genetics of HypertensionR01HL076709 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI JOE, BINA · 2008 to 2011
$1.6M
BIOCHEMISTRY AND GENETICS OF HYPERTENSIONR37HL020176 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI RAPP, JOHN P · 1993 to 2002
$1.6M
NHLBI NIH HHS HL020176NHLBI NIH HHS HL076709NHLBI NIH HHS R01 HL020176NHLBI NIH HHS R01 HL076709NHLBI NIH HHS R37 HL020176
6 · The paper itself

Abstract

Previously linkage and substitution mapping were conducted between the Dahl Salt-sensitive (S) rat and the Spontaneously Hypertensive Rat (SHR) to address the hypothesis that genetic contributions to blood pressure (BP) in two genetically hypertensive rat strains are different. Among the BP quantitative trait loci (QTLs) detected, two are located on chromosome 9 within large genomic segments. The goal of the current study was to develop new iterations of congenic substrains, to further resolve both of these BP QTLs on chromosome 9 as independent congenic segments. A total of 10 new congenic substrains were developed and characterized. The newly developed congenic substrains S.SHR(9)x8Ax11A and S.SHR(9)x10Ax1, with introgressed segments of 2.05 and 6.14 Mb, represented the shortest genomic segments. Both of these congenic substrains, S.SHR(9)x8Ax11A and S.SHR(9)x10Ax1 lowered BP of the S rat by 56 mm Hg (P<0.001) and 15 mm Hg (P<0.039), respectively. The BP measurements were corroborated by radiotelemetry. Urinary protein excretion was significantly lowered by SHR alleles within S.SHR(9)x10Ax1 but not by S.SHR(9)x8Ax11A. The shorter of the two congenic segments, 2.05 Mb was further characterized and found to contain a single differentially expressed protein-coding gene, Tomoregulin-2 (Tmeff2). The protein expression of Tmeff2 was higher in the S rat compared with S.SHR(9)x8Ax11A, which also had lower cardiac hypertrophy as measured by echocardiography. Tmeff2 is known to be upregulated in patients from multiple cohorts with cardiac hypertrophy. Taken together, Tmeff2 can be prioritized as a candidate gene for hypertension and associated cardiac hypertrophy in both rats and in humans.

Indexed as

AgingAnimalsAnimals, CongenicBlood PressureBlotting, WesternBody WeightChromosome MappingDNAEchocardiographyGenetic LociHypertensionMembrane GlycoproteinsMicrosatellite RepeatsOrgan SizeProteinuriaRatsDNAMembrane GlycoproteinsRNAtomoregulin-2, rat

Identifiers

PMID21814219
PMCPMC3808166
OpenAlexW2035315246

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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.