Evidence map›Paper›PMID 36129958›Full record

ArticlePloS one2022

Epigenetic analysis in placentas from sickle cell disease patients reveals a hypermethylation profile.

Gislene Pereira Gil, Galina Ananina, Mariana Maschietto, Sheila Coelho Soares Lima, Sueli Matilde da Silva Costa, Leticia de Carvalho Baptista, Mirta Tomie Ito, Fernando Ferreira Costa, Maria Laura Costa, Mônica Barbosa de Melo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. 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

10 authors at 3 institutions in 1 country.

Gislene Pereira GilCenter for Molecular Biology and Genetic Engineering (CBMEG), University of Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Galina AnaninaCenter for Molecular Biology and Genetic Engineering (CBMEG), University of Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Mariana MaschiettoBoldrini Children's Center, Campinas, São Paulo, Brazil.ORCID 0000-0003-2589-3186
Sheila Coelho Soares LimaNational Cancer Institute (INCA), Rio de Janeiro, Rio de Janeiro, Brazil.
Sueli Matilde da Silva CostaCenter for Molecular Biology and Genetic Engineering (CBMEG), University of Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Leticia de Carvalho BaptistaCenter for Molecular Biology and Genetic Engineering (CBMEG), University of Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Mirta Tomie ItoCenter for Molecular Biology and Genetic Engineering (CBMEG), University of Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Fernando Ferreira CostaHematology and Hemotherapy Center, University of Campinas, Campinas, São Paulo, Brazil.
Maria Laura CostaDepartment of Obstetrics and Gynecology, University of Campinas, Campinas, São Paulo, Brazil.
Mônica Barbosa de MeloCenter for Molecular Biology and Genetic Engineering (CBMEG), University of Campinas-UNICAMP, Campinas, São Paulo, Brazil.ORCID 0000-0002-1801-5441
Universidade Estadual de Campinas (UNICAMP) · BRCentro Infantil Boldrini · BRInstituto Nacional de Câncer - INCA · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pregnancy in Sickle Cell Disease (SCD) women is associated to increased risk of clinical and obstetrical complications. Placentas from SCD pregnancies can present increased abnormal findings, which may lead to placental insufficiency, favoring adverse perinatal outcome. These placental abnormalities are well known and reported, however little is known about the molecular mechanisms, such as epigenetics. Thus, our aim was to evaluate the DNA methylation profile in placentas from women with SCD (HbSS and HbSC genotypes), compared to uncomplicated controls (HbAA). We included in this study 11 pregnant women with HbSS, 11 with HbSC and 21 with HbAA genotypes. Illumina Methylation EPIC BeadChip was used to assess the whole placental DNA methylation. Pyrosequencing was used for array data validation and qRT-PCR was applied for gene expression analysis. Our results showed high frequency of hypermethylated CpGs sites in HbSS and HbSC groups with 73.5% and 76.2% respectively, when compared with the control group. Differentially methylated regions (DMRs) also showed an increased hypermethylation status for the HbSS (89%) and HbSC (86%) groups, when compared with the control group methylation data. DMRs were selected for methylation validation (4 DMRs-HbSS and 3 DMRs the HbSC groups) and after analyses three were validated in the HbSS group, and none in the HbSC group. The gene expression analysis showed differential expression for the PTGFR (-2.97-fold) and GPR56 (3.0-fold) genes in the HbSS group, and for the SPOCK1 (-2.40-fold) and ADCY4 (1.80-fold) genes in the HbSC group. Taken together, these data strongly suggest that SCD (HbSS and HbSC genotypes) can alter placental DNA methylation and lead to gene expression changes. These changes possibly contribute to abnormal placental development and could impact in the clinical course, especially for the fetus, possibly leading to increased risk of abortion, fetal growth restriction (FGR), stillbirth, small for gestational age newborns and prematurity.

Indexed as

Anemia, Sickle CellHemoglobin SC DiseaseEpigenesis, GeneticFemaleHemoglobin, SickleHumansInfant, NewbornPlacentaPregnancyProteoglycansHemoglobin, SickleProteoglycansSPOCK1 protein, human

Identifiers

PMID36129958
PMCPMC9491616
OpenAlexW4296810513

What OpenQuestion holds

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Registered trials

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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.