Evidence map›Paper›PMID 19538749›Full record

ArticleBMC genomics2009

Maternal diabetes alters transcriptional programs in the developing embryo.

Gabriela Pavlinkova, J Michael Salbaum, Claudia Kappen

Abstract read
In one paragraph

Article in BMC genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
–field-weighted citation impact
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

66 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Mitochondrial Dysfunction in Congenital Heart Disease.Journal of cardiovascular development and disease · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Differential responses to maternal diabetes in embryo and visceral yolk sac.Frontiers in cell and developmental biology · 2023
    Article
  10. Article
  11. Article
  12. Observational
  13. Article
  14. Review
  15. Article
  16. Review
  17. Epigenetic Changes in Gestational Diabetes Mellitus.International journal of molecular sciences · 2021
    Review
  18. Review
  19. Review
  20. Review

6 more citing papers are in PubMed but not listed here.

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

3 authors.

Gabriela PavlinkovaDepartment of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE 68198-5455, USA. gpavlinkova@img.cas.cz
J Michael Salbaum
Claudia Kappen

Funding

ZINC FINGER-INSPIRED FLUORESCENT CHEMOSENSORSP20RR016469 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI TURPEN, JAMES B · 2001 to 2011
$36.2M
Research BaseP30DK072476 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Peter Todd Katzmarzyk · 2005 to 2026
$26.5M
TRANSGENIC EXPRESSION ANALYSIS OF MIRNA-144P20RR018788 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI NYSTUEN, ARNE M · 2003 to 2011
$16.5M
MOLECULAR MECHANISMS IN DIABETIC EMBRYOPATHYR01HD037804 · NICHD · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI KAPPEN, CLAUDIA T · 1998 to 2010
$2.5M
Neural tube defects in diabetic pregnancyR01HD055528 · NICHD · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI SALBAUM, J MICHAEL · 2007 to 2011
$1.8M
MOLECULAR BASIS OF ENTEROCYTE REGULATION DURING ONTOGENYR01HD034706 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARTIN, MARTIN G · 1998 to 2002
$546k
NCRR NIH HHS P20 RR016469NCRR NIH HHS P20RR016469NCRR NIH HHS P20 RR018788NCRR NIH HHS P20RR018788NICHD NIH HHS R01 HD034706NICHD NIH HHS R01 HD037804NICHD NIH HHS R01 HD055528NICHD NIH HHS R01-HD055528NICHD NIH HHS R01-HD34706NIDDK NIH HHS P30 DK072476
6 · The paper itself

Abstract

backgroundMaternal diabetes is a well-known risk factor for birth defects, such as heart defects and neural tube defects. The causative molecular mechanisms in the developing embryo are currently unknown, and the pathogenesis of developmental abnormalities during diabetic pregnancy is not well understood. We hypothesized that the developmental defects are due to alterations in critical developmental pathways, possibly as a result of altered gene expression. We here report results from gene expression profiling of exposed embryos from a mouse diabetes model.

resultsIn comparison to normal embryos at mid-gestation, we find significantly altered gene expression levels in diabetes-exposed embryos. Independent validation of altered expression was obtained by quantitative Real Time Polymerase Chain Reaction. Sequence motifs in the promoters of diabetes-affected genes suggest potential binding of transcription factors that are involved in responses to oxidative stress and/or to hypoxia, two conditions known to be associated with diabetic pregnancies. Functional annotation shows that a sixth of the de-regulated genes have known developmental phenotypes in mouse mutants. Over 30% of the genes we have identified encode transcription factors and chromatin modifying proteins or components of signaling pathways that impinge on transcription.

conclusionExposure to maternal diabetes during pregnancy alters transcriptional profiles in the developing embryo. The enrichment, within the set of de-regulated genes, of those encoding transcriptional regulatory molecules provides support for the hypothesis that maternal diabetes affects specific developmental programs.

Indexed as

Gene Expression ProfilingAnimalsBinding SitesDiabetes Mellitus, ExperimentalEmbryo, MammalianEmbryonic DevelopmentFemaleGene Expression Regulation, DevelopmentalMiceOligonucleotide Array Sequence AnalysisPregnancyTranscription FactorsTranscription Factors

Identifiers

PMID19538749
PMCPMC2715936

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.