Evidence map›Paper›PMID 27019630›Full record

ArticleInternational journal of biological sciences2016

Hyperglycemia Differentially Affects Maternal and Fetal DNA Integrity and DNA Damage Response.

Jusciele B Moreli, Janine H Santos, Aline Rodrigues Lorenzon-Ojea, Simone Corrêa-Silva, Rodrigo S Fortunato, Clarissa Ribeiro Rocha, Marilza V Rudge, Débora C Damasceno, Estela Bevilacqua, Iracema M Calderon

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2016. 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
3.7field-weighted citation impact, top 8% 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, 28 citations in OpenAlex.

  1. Trial
  2. Article
  3. Association between Maternal Blood Glucose Levels during Pregnancy and Birth Outcomes: A Birth Cohort Study.International journal of environmental research and public health · 2023
    Article
  4. Review
  5. 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

10 authors at 4 institutions in 4 countries.

Jusciele B Moreli1. Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University / UNESP, São Paulo, Brazil.
Janine H Santos2. Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences / NIEHS, North Carolina, USA.
Aline Rodrigues Lorenzon-Ojea3. Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo / USP, São Paulo, Brazil.
Simone Corrêa-Silva1. Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University / UNESP, São Paulo, Brazil.; 3. Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo / USP, São Paulo, Brazil.
Rodrigo S Fortunato4. Laboratory of Molecular Radiobiology, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro / UFRJ, Rio de Janeiro, Brazil.
Clarissa Ribeiro Rocha5. DNA Repair Laboratory, Department of Microbiology, Institute of Biomedical Sciences, University of São Paulo / USP, São Paulo, Brazil.
Marilza V Rudge1. Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University / UNESP, São Paulo, Brazil.
Débora C Damasceno1. Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University / UNESP, São Paulo, Brazil.
Estela Bevilacqua3. Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo / USP, São Paulo, Brazil.
Iracema M Calderon1. Graduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University / UNESP, São Paulo, Brazil.
Institute of Biomedical Science · GBUniversidade Estadual Paulista (Unesp) · BRCzech Academy of Sciences, Institute of Biophysics · CZNational Institute of Environmental Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveInvestigate the DNA damage and its cellular response in blood samples from both mother and the umbilical cord of pregnancies complicated by hyperglycemia.

methodsA total of 144 subjects were divided into 4 groups: normoglycemia (ND; 46 cases), mild gestational hyperglycemia (MGH; 30 cases), gestational diabetes mellitus (GDM; 45 cases) and type-2 diabetes mellitus (DM2; 23 cases). Peripheral blood mononuclear cell (PBMC) isolation and/or leukocytes from whole maternal and umbilical cord blood were obtained from all groups at delivery. Nuclear and mitochondrial DNA damage were measured by gene-specific quantitative PCR, and the expression of mRNA and proteins involved in the base excision repair (BER) pathway were assessed by real-time qPCR and Western blot, respectively. Apoptosis was measured in vitro experiments by caspase 3/7 activity and ATP levels.

resultsGDM and DM2 groups were characterized by an increase in oxidative stress biomarkers, an increase in nuclear and mitochondrial DNA damage, and decreased expression of mRNA (APE1, POLβ and FEN1) and proteins (hOGG1, APE1) involved in BER. The levels of hyperglycemia were associated with the in vitro apoptosis pathway. Blood levels of DNA damage in umbilical cord were similar among the groups. Newborns of diabetic mothers had increased expression of BER mRNA (APE1, POLβ and FEN1) and proteins (hOGG1, APE1, POLβ and FEN1). A diabetes-like environment was unable to induce apoptosis in the umbilical cord blood cells.

conclusionsOur data show relevant asymmetry between maternal and fetal blood cell susceptibility to DNA damage and apoptosis induction. Maternal cells seem to be more predisposed to changes in an adverse glucose environment. This may be due to differential ability in upregulating multiple genes involved in the activation of DNA repair response, especially the BER mechanism. However if this study shows a more effective adaptive response by the fetal organism, it also calls for further studies to determine the limit of this response that definitely changes the fate of a fetus under these conditions of cellular stress.

Indexed as

Diabetes, GestationalDiabetes Mellitus, Type 2DNA-(Apurinic or Apyrimidinic Site) LyaseDNA DamageDNA GlycosylasesDNA RepairFemaleFlap EndonucleasesHumansHyperglycemiaPregnancyAPEX1 protein, humanDNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesFlap Endonucleasesoxoguanine glycosylase 1, humanDiabetesDNA damageDNA repair.Pregnancy

Identifiers

PMID27019630
PMCPMC4807165
OpenAlexW2322428758

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.