Evidence map›Paper›PMID 18028541›Full record

ArticleBMC developmental biology2007

Differentially expressed genes in embryonic cardiac tissues of mice lacking Folr1 gene activity.

Huiping Zhu, Robert M Cabrera, Bogdan J Wlodarczyk, Daniel Bozinov, Deli Wang, Robert J Schwartz, Richard H Finnell

Open access · hybridAbstract read
In one paragraph

Article in BMC developmental biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Folic acid supplementation on congenital heart disease and its dual character.Current research in pharmacology and drug discovery · 2025
    Review
  2. Article
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  7. Mutations in folate transporter genes and risk for human myelomeningocele.American journal of medical genetics. Part A · 2017
    Article
  8. Article
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  10. Molecular mechanisms underlying the potentially adverse effects of folate.Clinical chemistry and laboratory medicine · 2013
    Review
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  17. Review
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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

7 authors at 2 institutions in 1 country.

Huiping ZhuCenter for Environmental and Genetic Medicine, Institute of Biosciences and Technology, Texas A&M University System Health Science Center, Houston, Texas 77030, USA. hzhu@ibt.tamhsc.edu
Robert M Cabrera
Bogdan J Wlodarczyk
Daniel Bozinov
Deli Wang
Robert J Schwartz
Richard H Finnell
Texas A&M University System · USUniversity of Alabama at Birmingham · US

Funding

Interaction of teratogens in heart developmentP01HL066398 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BENNETT, GREGORY D · 2001 to 2005
$5.6M
NHLBI NIH HHS 1P01HL66398NHLBI NIH HHS P01 HL066398
6 · The paper itself

Abstract

backgroundHeart anomalies are the most frequently observed among all human congenital defects. As with the situation for neural tube defects (NTDs), it has been demonstrated that women who use multivitamins containing folic acid peri-conceptionally have a reduced risk for delivering offspring with conotruncal heart defects 123. Cellular folate transport is mediated by a receptor or binding protein and by an anionic transporter protein system. Defective function of the Folr1 (also known as Folbp1; homologue of human FRalpha) gene in mice results in inadequate transport, accumulation, or metabolism of folate during cardiovascular morphogenesis.

resultsWe have observed cardiovascular abnormalities including outflow tract and aortic arch arterial defects in genetically compromised Folr1 knockout mice. In order to investigate the molecular mechanisms underlying the failure to complete development of outflow tract and aortic arch arteries in the Folr1 knockout mouse model, we examined tissue-specific gene expression difference between Folr1 nullizygous embryos and morphologically normal heterozygous embryos during early cardiac development (14-somite stage), heart tube looping (28-somite stage), and outflow track septation (38-somite stage). Microarray analysis was performed as a primary screening, followed by investigation using quantitative real-time PCR assays. Gene ontology analysis highlighted the following ontology groups: cell migration, cell motility and localization of cells, structural constituent of cytoskeleton, cell-cell adhesion, oxidoreductase, protein folding and mRNA processing. This study provided preliminary data and suggested potential candidate genes for further description and investigation.

conclusionThe results suggested that Folr1 gene ablation and abnormal folate homeostasis altered gene expression in developing heart and conotruncal tissues. These changes affected normal cytoskeleton structures, cell migration and motility as well as cellular redox status, which may contribute to cardiovascular abnormalities in mouse embryos lacking Folr1 gene activity.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsEmbryo, MammalianFemaleFolate Receptor 1Gene Expression ProfilingHeartHeart Defects, CongenitalMaleMiceMice, KnockoutOligonucleotide Array Sequence AnalysisPregnancyReceptors, Cell SurfaceReverse Transcriptase Polymerase Chain ReactionFolate Receptor 1Folr1 protein, mouseReceptors, Cell Surface

Identifiers

PMID18028541
PMCPMC2206038
OpenAlexW1965721643

What OpenQuestion holds

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LicenceCC BY
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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.