Evidence map›Paper›PMID 20926892›Full record

ArticleJournal of vascular research2011

Induced chromosome deletion in a Williams-Beuren syndrome mouse model causes cardiovascular abnormalities.

Craig J Goergen, Hong-Hua Li, Uta Francke, Charles A Taylor

Open access · bronzeAbstract read
In one paragraph

Article in Journal of vascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
  2. Elastin, arterial mechanics, and stenosis.American journal of physiology. Cell physiology · 2022
    Review
  3. Article
  4. Review
  5. Article
  6. Elastin, arterial mechanics, and cardiovascular disease.American journal of physiology. Heart and circulatory physiology · 2018
    Review
  7. ACS biomaterials science & engineering · 2017
    Article
  8. Article
  9. Review
  10. Article
  11. Comparison of Traditional and Integrated Digital Anesthetic Vaporizers.Journal of the American Association for Laboratory Animal Science : JAALAS · 2015
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

4 authors at 2 institutions in 2 countries.

Craig J GoergenDepartment of Bioengineering, Stanford University School of Medicine, Stanford, Calif., USA. cgoergen@stanford.edu
Hong-Hua Li
Uta Francke
Charles A Taylor
Bioengineering Center · RUStanford University · US

Funding

Function of Genes in Williams Syndrome Deletion RegionR01HD039927 · NICHD · STANFORD UNIVERSITY · PI FRANCKE, UTA · 2001 to 2005
$2.2M
NICHD NIH HHS R01 HD039927NICHD NIH HHS R01HD39927
6 · The paper itself

Abstract

aimsThe Williams-Beuren syndrome (WBS) is a genetic disorder caused by a heterozygous ~1.5-Mb deletion. The aim of this study was to determine how the genetic changes in a Wbs mouse model alter Eln expression, blood pressure, vessel structure, and abdominal aortic wall dynamics in vivo.

methodsElastin (ELN) transcript levels were quantified by qRT-PCR and blood pressure was measured with a tail cuff system. M-mode ultrasound was used to track pulsatile abdominal aortic wall motion. Aortas were sectioned and stained to determine medial lamellar structure.

resultsELN transcript levels were reduced by 38-41% in Wbs mice lacking one copy of the ELN gene. These mice also had a 10-20% increase in mean blood pressure and significantly reduced circumferential cyclic strain (p < 0.001). Finally, histological sections showed disorganized and fragmented elastin sheets in Wbs mice, but not the characteristic increase in lamellar units seen in Eln(+/-) mice.

conclusionsThe deletion of Eln in this Wbs mouse model results in lower gene expression, hypertension, reduced cyclic strain, and fragmented elastin sheets. The observation that the number of medial lamellar units is normal in Wbs deletion mice, which is in contrast to Eln(+/-) mice, suggests other genes may be involved in vascular development.

Indexed as

Chromosome DeletionAnimalsAorta, AbdominalBlood PressureCardiovascular AbnormalitiesDisease Models, AnimalElasticityElastinFemaleGene ExpressionMaleMiceMice, Inbred C57BLPhenotypeUltrasonographyWilliams SyndromeElastin

Identifiers

PMID20926892
PMCPMC2975735
OpenAlexW1982500276

What OpenQuestion 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 OpenQuestion graph.