Evidence map›Paper›PMID 24768206›Full record

ArticleJournal of diabetes and its complications

Gestational diabetes mellitus alters apoptotic and inflammatory gene expression of trophobasts from human term placenta.

Thomas R Magee, Michael G Ross, Lauren Wedekind, Mina Desai, Siri Kjos, Louiza Belkacemi

Open access · greenAbstract read
In one paragraph

Article in Journal of diabetes and its complications. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
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  10. The role of microRNAs in pregnancies complicated by maternal diabetes.Clinical science (London, England : 1979) · 2024
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  20. Human Chorionic Villous Differentiation and Placental Development.International journal of molecular sciences · 2022
    Review
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.

Thomas R MageeDepartment of Obstetrics and Gynecology, Perinatal Research Laboratories, David Geffen School of Medicine at University of California in Los Angeles, Los Angeles, CA, USA; Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA; Department of Health and Life Sciences at Charles R. Drew University of Medicine and Science, Los Angeles, CA, USA.
Michael G RossDepartment of Obstetrics and Gynecology, Perinatal Research Laboratories, David Geffen School of Medicine at University of California in Los Angeles, Los Angeles, CA, USA; Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA.
Lauren WedekindLos Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA.
Mina DesaiDepartment of Obstetrics and Gynecology, Perinatal Research Laboratories, David Geffen School of Medicine at University of California in Los Angeles, Los Angeles, CA, USA; Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA.
Siri KjosDepartment of Obstetrics and Gynecology, Perinatal Research Laboratories, David Geffen School of Medicine at University of California in Los Angeles, Los Angeles, CA, USA.
Louiza BelkacemiDepartment of Obstetrics and Gynecology, Perinatal Research Laboratories, David Geffen School of Medicine at University of California in Los Angeles, Los Angeles, CA, USA; Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA. Electronic address: lbelkacemi1@gmail.com.
University of California, Los Angeles · USThe Lundquist Institute · USCharles R. Drew University of Medicine and Science · US

Funding

ZONA-FREE HAMSTER OVA ASSAY AS AN INDICATOR OF MALE FERTILITYM01RR000425 · NCRR · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI ANDERSON, GAIL V · 1985 to 2011
$74.2M
Workshop for Junior Biostatisticians in Health ResearchU54MD007598 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI Jaydutt V. Vadgama · 2012 to 2026
$60.0M
Gestational Programming of NephrogenesisR03HD060782 · NICHD · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI MAGEE, THOMAS R · 2010 to 2011
$151k
NCRR NIH HHS M01 RR000425NCRR NIH HHS M01RR000425NICHD NIH HHS R03 HD060782NICHD NIH HHS R03 HD060782-02NIMHD NIH HHS U54 MD007598PHS HHS NHG0811K15-AXIS-PILOT-15
6 · The paper itself

Abstract

aimIncreased placental growth secondary to reduced apoptosis may contribute to the development of macrosomia in GDM pregnancies. We hypothesize that reduced apoptosis in GDM placentas is caused by dysregulation of apoptosis related genes from death receptors or mitochondrial pathway or both to enhance placental growth in GDM pregnancies.

methodsNewborn and placental weights from women with no pregnancy complications (controls; N=5), or with GDM (N=5) were recorded. Placental villi from both groups were either fixed for TUNEL assay, or snap frozen for gene expression analysis by apoptosis PCR microarrays and qPCR.

resultsMaternal, placental and newborn weights were significantly higher in the GDM group vs. Controls. Apoptotic index of placentas from the GDM group was markedly lower than the Controls. At a significant threshold of 1.5, seven genes (BCL10, BIRC6, BIRC7, CASP5, CASP8P2, CFLAR, and FAS) were down regulated, and 13 genes (BCL2, BCL2L1, BCL2L11, CASP4, DAPK1, IκBκE, MCL1, NFκBIZ, NOD1, PEA15, TNF, TNFRSF25, and XIAP) were unregulated in the GDM placentas. qPCR confirmed the consistency of the PCR microarray. Using Western blotting we found significantly decreased placental pro-apoptotic FAS receptor and FAS ligand (FASL), and increased mitochondrial anti-apoptotic BCL2 post GDM insult. Notably, caspase-3, which plays a central role in the execution-phase of apoptosis, and its substrate poly (ADP-ribose) polymerase (PARP) were significantly down regulated in GDM placentas, as compared to non-diabetic Control placentas.

conclusionMaternal GDM results in heavier placentas with aberrant placental apoptotic and inflammatory gene expression that may account, at least partially, for macrosomia in newborns.

Indexed as

ApoptosisGene Expression Regulation, DevelopmentalModels, BiologicalAdultApoptosis Regulatory ProteinsBirth WeightDiabetes, GestationalFemaleFetal MacrosomiaGene Expression ProfilingHumansInflammation MediatorsOligonucleotide Array Sequence AnalysisPlacentaPlacentationPregnancyApoptosis Regulatory ProteinsInflammation MediatorsRNA, MessengerApoptosisApoptotic gene microarrayGestational diabetesPlacenta

Identifiers

PMID24768206
PMCPMC4166519
OpenAlexW2127937089

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.