Evidence map›Paper›PMID 32009522›Full record

ArticleJournal of the American Heart Association2020

Angiogenesis-Related Genes in Endothelial Progenitor Cells May Be Involved in Sickle Cell Stroke.

Mirta T Ito, Sueli M da Silva Costa, Letícia C Baptista, Gabriela Q Carvalho-Siqueira, Dulcinéia M Albuquerque, Vinicius M Rios, Stephanie Ospina-Prieto, Roberta C Saez, Karla P Vieira, Fernando Cendes and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Stroke and presence of patent foramen ovale in sickle cell disease.Journal of thrombosis and thrombolysis · 2021
    Review
  7. Article
  8. Review
  9. 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

14 authors at 1 institution in 1 country.

Mirta T ItoCenter for Molecular Biology and Genetic Engineering University of Campinas-UNICAMP Campinas São Paulo Brazil.
Sueli M da Silva CostaCenter for Molecular Biology and Genetic Engineering University of Campinas-UNICAMP Campinas São Paulo Brazil.
Letícia C BaptistaCenter for Molecular Biology and Genetic Engineering University of Campinas-UNICAMP Campinas São Paulo Brazil.
Gabriela Q Carvalho-SiqueiraCenter for Molecular Biology and Genetic Engineering University of Campinas-UNICAMP Campinas São Paulo Brazil.
Dulcinéia M AlbuquerqueHematology and Hemotherapy Center University of Campinas-UNICAMP Campinas São Paulo Brazil.
Vinicius M RiosCenter for Molecular Biology and Genetic Engineering University of Campinas-UNICAMP Campinas São Paulo Brazil.
Stephanie Ospina-PrietoHematology and Hemotherapy Center University of Campinas-UNICAMP Campinas São Paulo Brazil.
Roberta C SaezHematology and Hemotherapy Center University of Campinas-UNICAMP Campinas São Paulo Brazil.
Karla P VieiraHematology and Hemotherapy Center University of Campinas-UNICAMP Campinas São Paulo Brazil.
Fernando CendesNeuroimaging Laboratory Department of Neurology University of Campinas, UNICAMP Campinas São Paulo Brazil.
Margareth C OzeloHematology and Hemotherapy Center University of Campinas-UNICAMP Campinas São Paulo Brazil.
Sara Teresinha O SaadHematology and Hemotherapy Center University of Campinas-UNICAMP Campinas São Paulo Brazil.
Fernando F CostaHematology and Hemotherapy Center University of Campinas-UNICAMP Campinas São Paulo Brazil.
Mônica B MeloCenter for Molecular Biology and Genetic Engineering University of Campinas-UNICAMP Campinas São Paulo Brazil.
Universidade Estadual de Campinas (UNICAMP) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background The clinical aspects of sickle cell anemia (SCA) are heterogeneous, and different patients may present significantly different clinical evolutions. Almost all organs can be affected, particularly the central nervous system. Transient ischemic events, infarcts, and cerebral hemorrhage can be observed and affect ≈25% of the patients with SCA. Differences in the expression of molecules produced by endothelial cells may be associated with the clinical heterogeneity of patients affected by vascular diseases. In this study, we investigated the differential expression of genes involved in endothelial cell biology in SCA patients with and without stroke. Methods and Results Endothelial progenitor cells from 4 SCA patients with stroke and 6 SCA patients without stroke were evaluated through the polymerase chain reaction array technique. The analysis of gene expression profiling identified 29 differentially expressed genes. Eleven of these genes were upregulated, and most were associated with angiogenesis (55%), inflammatory response (18%), and coagulation (18%) pathways. Downregulated expression was observed in 18 genes, with the majority associated with angiogenesis (28%), apoptosis (28%), and cell adhesion (22%) pathways. Remarkable overexpression of the

Indexed as

Neovascularization, PhysiologicAdultAnemia, Sickle CellAngiogenic ProteinsCase-Control StudiesEndothelial Progenitor CellsFemaleHumansMaleMatrix Metalloproteinase 1Middle AgedStrokeTranscriptomeAngiogenic ProteinsMatrix Metalloproteinase 1MMP1 protein, humangene expressionMMP1sickle cell anemiastroke

Identifiers

PMID32009522
PMCPMC7033889
OpenAlexW3004492879

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.