Evidence map›Paper›PMID 38386032›Full record

ArticleAnnals of hematology2024

Comparative transcriptomic analysis of circulating endothelial cells in sickle cell stroke.

Júlia Nicoliello Pereira de Castro, Sueli Matilde da Silva Costa, Ana Carolina Lima Camargo, Mirta Tomie Ito, Bruno Batista de Souza, Victor de Haidar E Bertozzo, Thiago Adalton Rosa Rodrigues, Carolina Lanaro, Dulcinéia Martins de Albuquerque, Roberta Casagrande Saez and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Annals of hematology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

15 authors at 1 institution in 1 country.

Júlia Nicoliello Pereira de CastroLaboratory of Human Genetics, Center for Molecular Biology and Genetic Engineering-CBMEG, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, 13083-875, Brazil.
Sueli Matilde da Silva CostaLaboratory of Human Genetics, Center for Molecular Biology and Genetic Engineering-CBMEG, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, 13083-875, Brazil.
Ana Carolina Lima CamargoLaboratory of Human Genetics, Center for Molecular Biology and Genetic Engineering-CBMEG, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, 13083-875, Brazil.
Mirta Tomie ItoLaboratory of Human Genetics, Center for Molecular Biology and Genetic Engineering-CBMEG, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, 13083-875, Brazil.
Bruno Batista de SouzaLaboratory of Human Genetics, Center for Molecular Biology and Genetic Engineering-CBMEG, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, 13083-875, Brazil.
Victor de Haidar E BertozzoLaboratory of Human Genetics, Center for Molecular Biology and Genetic Engineering-CBMEG, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, 13083-875, Brazil.
Thiago Adalton Rosa RodriguesLaboratory of Human Genetics, Center for Molecular Biology and Genetic Engineering-CBMEG, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, 13083-875, Brazil.
Carolina LanaroHematology and Hemotherapy Center, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Dulcinéia Martins de AlbuquerqueHematology and Hemotherapy Center, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Roberta Casagrande SaezHematology and Hemotherapy Center, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Sara Teresinha Olalla SaadHematology and Hemotherapy Center, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Margareth Castro OzeloHematology and Hemotherapy Center, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Fernando CendesNeuroimaging Laboratory, Department of Neurology, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Fernando Ferreira CostaHematology and Hemotherapy Center, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, Brazil.
Mônica Barbosa de MeloLaboratory of Human Genetics, Center for Molecular Biology and Genetic Engineering-CBMEG, Universidade Estadual de Campinas-UNICAMP, Campinas, São Paulo, 13083-875, Brazil. melomb@unicamp.br.ORCID http://orcid.org/0000-0002-1801-5441
Universidade Estadual de Campinas (UNICAMP) · BR

Funding

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Finance code 001Fundação de Amparo à Pesquisa do Estado de São Paulo 2014/00984-3Fundação de Amparo à Pesquisa do Estado de São Paulo 2019/18886-1Fundação de Amparo à Pesquisa do Estado de São Paulo 2021/14089-0
6 · The paper itself

Abstract

Ischemic stroke (IS) is one of the most impairing complications of sickle cell anemia (SCA), responsible for 20% of mortality in patients. Rheological alterations, adhesive properties of sickle reticulocytes, leukocyte adhesion, inflammation and endothelial dysfunction are related to the vasculopathy observed prior to ischemic events. The role of the vascular endothelium in this complex cascade of mechanisms is emphasized, as well as in the process of ischemia-induced repair and neovascularization. The aim of the present study was to perform a comparative transcriptomic analysis of endothelial colony-forming cells (ECFCs) from SCA patients with and without IS. Next, to gain further insights of the biological relevance of differentially expressed genes (DEGs), functional enrichment analysis, protein-protein interaction network (PPI) construction and in silico prediction of regulatory factors were performed. Among the 2469 DEGs, genes related to cell proliferation (AKT1, E2F1, CDCA5, EGFL7), migration (AKT1, HRAS), angiogenesis (AKT1, EGFL7) and defense response pathways (HRAS, IRF3, TGFB1), important endothelial cell molecular mechanisms in post ischemia repair were identified. Despite the severity of IS in SCA, widely accepted molecular targets are still lacking, especially related to stroke outcome. The comparative analysis of the gene expression profile of ECFCs from IS patients versus controls seems to indicate that there is a persistent angiogenic process even after a long time this complication has occurred. Thus, this is an original study which may lead to new insights into the molecular basis of SCA stroke and contribute to a better understanding of the role of endothelial cells in stroke recovery.

Indexed as

Anemia, Sickle CellStrokeCalcium-Binding ProteinsEGF Family of ProteinsEndothelial CellsGene Expression ProfilingHumansIschemiaTranscriptomeCalcium-Binding ProteinsEGF Family of ProteinsEGFL7 protein, humanEndothelial colony-forming cellsIschemic strokeRNA-SeqSickle cell anemia

Identifiers

PMID38386032
OpenAlexW4392055178

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.