Evidence map›Paper›PMID 25826117›Full record

ArticlePediatric research2015

IUGR prevents IGF-1 upregulation in juvenile male mice by perturbing postnatal IGF-1 chromatin remodeling.

Camille M Fung, Yueqin Yang, Qi Fu, Ashley S Brown, Baifeng Yu, Christopher W Callaway, Jicheng Li, Robert H Lane, Robert A McKnight

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Pediatric research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

9 authors at 3 institutions in 2 countries.

Camille M FungDivision of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
Yueqin Yang1] Division of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah [2] Institute of Cell Biology, Zhejiang University, Hangzhou, Zhejiang, China.
Qi FuDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin.
Ashley S BrownDivision of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
Baifeng YuDivision of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
Christopher W CallawayDivision of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
Jicheng LiInstitute of Cell Biology, Zhejiang University, Hangzhou, Zhejiang, China.
Robert H LaneDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin.
Robert A McKnightDivision of Neonatology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
University of Utah · USMedical College of Wisconsin · USZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntrauterine growth restriction (IUGR) offspring with rapid catch-up growth are at increased risk for early obesity especially in males. Persistent insulin-like growth factor-1 (IGF-1) reduction is an important risk factor. Using a mouse model of maternal hypertension-induced IUGR, we examined IGF-1 levels, promoter DNA methylation, and histone H3 covalent modifications at birth (D1). We additionally investigated whether prenatal perturbations could reset at preadolescence (D21).

methodsIUGR was induced via maternal thromboxane A2-analog infusion in mice.

resultsIUGR uniformly decreased D1 IGF-1 mRNA and protein levels with reduced promoter 1 (P1) transcription and increased P1 DNA methylation. IUGR males also had increased H3K4ac at exon 5 and 3' distal UTR. At D21, IUGR males continued to have decreased IGF-1 levels, originating from both P1 and P2 with reduced 1A variant. IUGR males also had decreased activation mark of H3K4me3 at P1 compared with sham males. In contrast, D21 IUGR females normalized their IGF-1 levels, in association with an increased activation mark of H3K4me3 at P1 compared with sham females.

conclusionIUGR uniformly affected D1 hepatic IGF-1 epigenetic modifications in both sexes. However, at preadolescence, IUGR males are unable to correct for the prenatal reduction possibly due to a more perturbed IGF-1 chromatin structure.

Indexed as

Chromatin Assembly and DisassemblyGene Expression Regulation, DevelopmentalAnimalsBlood GlucoseBody WeightChromatinDNA MethylationExonsFemaleFetal Growth RetardationHistonesInsulinInsulin-Like Growth Factor ILiverMaleMiceBlood GlucoseChromatinHistonesInsulininsulin-like growth factor-1, mouseInsulin-Like Growth Factor IThromboxane A2

Identifiers

PMID25826117
OpenAlexW1969737996

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.