Evidence map›Paper›PMID 27599633›Full record

ArticleInternational journal of obesity (2005)2016

Bone marrow mesenchymal stem cells of the intrauterine growth-restricted rat offspring exhibit enhanced adipogenic phenotype.

Ming Gong, Sahaya Antony, Reiko Sakurai, Jie Liu, Michelina Iacovino, Virender K Rehan

Abstract read
In one paragraph

Article in International journal of obesity (2005), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  3. Review
  4. Review
  5. Article
  6. Maternal food restriction-induced intrauterine growth restriction in a rat model leads to sex-specific adipogenic programming.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  7. Article
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  9. Review
  10. Article
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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

6 authors at 3 institutions in 1 country.

Ming Gong *Department of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, David Geffen School of Medicine, Torrance, CA, USA.
Sahaya Antony *Department of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, David Geffen School of Medicine, Torrance, CA, USA.
Reiko SakuraiDepartment of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, David Geffen School of Medicine, Torrance, CA, USA.
Jie LiuDepartment of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, David Geffen School of Medicine, Torrance, CA, USA.
Michelina IacovinoDepartment of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, David Geffen School of Medicine, Torrance, CA, USA.
Virender K RehanDepartment of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, David Geffen School of Medicine, Torrance, CA, USA.
The Lundquist Institute · USUCLA Medical Center · USHarbor–UCLA Medical Center · US

Funding

Developmental Nicotine Exposure & Transgenerationally Altered Lung PhenotypeR01HL127237 · NHLBI · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI REHAN, VIRENDER K · 2016 to 2019
$1.8M
Molecular Basis of Childhood Asthma Following Perinatal Vitamin D DeficiencyR21HL107118 · NHLBI · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI REHAN, VIRENDER K · 2011 to 2012
$377k
In Utero Nicotine Exposure & Transgenerational Transmission of AsthmaR21HD071731 · NICHD · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI REHAN, VIRENDER K · 2012 to 2013
$369k
A Molecular Approach to Prevent Pulmonary Dysfunction in the Intrauterine GrowthR03HD058948 · NICHD · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI REHAN, VIRENDER K · 2009 to 2010
$137k
NHLBI NIH HHS R01 HL127237NHLBI NIH HHS R21 HL107118NICHD NIH HHS R03 HD058948NICHD NIH HHS R21 HD071731
6 · The paper itself

Abstract

objectiveAlthough intrauterine nutritional stress is known to result in offspring obesity and the metabolic phenotype, the underlying cellular/molecular mechanisms remain incompletely understood. We tested the hypothesis that compared with the controls, the bone marrow-derived mesenchymal stem cells (BMSCs) of the intrauterine growth-restricted (IUGR) offspring exhibit a more adipogenic phenotype.

methodsA well-established rat model of maternal food restriction (MFR), that is, 50% global caloric restriction during the later-half of pregnancy and ad libitum diet following birth that is known to result in an obese offspring with a metabolic phenotype was used. BMSCs at 3 weeks of age were isolated, and then molecularly and functionally profiled.

resultsBMSCs of the intrauterine nutritionally-restricted offspring demonstrated an increased proliferation and an enhanced adipogenic molecular profile at miRNA, mRNA and protein levels, with an overall up-regulated PPARγ (miR-30d, miR-103, PPARγ, C/EPBα, ADRP, LPL, SREBP1), but down-regulated Wnt (LRP5, LEF-1, β-catenin, ZNF521 and RUNX2) signaling profile. Following adipogenic induction, compared with the control BMSCs, the already up-regulated adipogenic profile of the MFR BMSCs, showed a further increased adipogenic response.

conclusionsMarkedly enhanced adipogenic molecular profile and increased cell proliferation of MFR BMSCs suggest a possible novel cellular/mechanistic link between the intrauterine nutritional stress and offspring metabolic phenotype. This provides new potential predictive and therapeutic targets against these conditions in the IUGR offspring.

Indexed as

AdipogenesisAnimalsAnimals, NewbornCaloric RestrictionCell DifferentiationDisease Models, AnimalDown-RegulationFemaleFetal Growth RetardationMaternal Nutritional Physiological PhenomenaMesenchymal Stem CellsMicroRNAsPeroxisome Proliferator-Activated ReceptorsPhenotypePregnancyRatsMicroRNAsPeroxisome Proliferator-Activated ReceptorsRNA, Messenger

Identifiers

PMID27599633
PMCPMC5113998
OpenAlexW2508755984

What OpenQuestion holds

Textmetadata
LicenceTDM
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.