Evidence map›Paper›PMID 25769545›Full record

ArticleHaematologica2015

Key endothelial cell angiogenic mechanisms are stimulated by the circulating milieu in sickle cell disease and attenuated by hydroxyurea.

Flavia C M Lopes, Fabiola Traina, Camila B Almeida, Flavia C Leonardo, Carla F Franco-Penteado, Vanessa T Garrido, Marina P Colella, Raquel Soares, Sara T Olalla-Saad, Fernando F Costa and 1 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  13. Increasing nitric oxide bioavailability fails to improve collateral vessel formation in humanized sickle cell mice.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
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  15. Article
  16. miR-29a-3p/THBS2 Axis Regulates PAH-Induced Cardiac Fibrosis.International journal of molecular sciences · 2021
    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

11 authors at 3 institutions in 2 countries.

Flavia C M LopesINCT de Sangue, Hematology Center, School of Medical Science, University of Campinas - UNICAMP, São Paulo, Brazil.
Fabiola TrainaINCT de Sangue, Hematology Center, School of Medical Science, University of Campinas - UNICAMP, São Paulo, Brazil Department of Internal Medicine, University of São Paulo at Riberão Preto Medical School, Riberão Preto, Brazil.
Camila B AlmeidaINCT de Sangue, Hematology Center, School of Medical Science, University of Campinas - UNICAMP, São Paulo, Brazil.
Flavia C LeonardoINCT de Sangue, Hematology Center, School of Medical Science, University of Campinas - UNICAMP, São Paulo, Brazil.
Carla F Franco-PenteadoINCT de Sangue, Hematology Center, School of Medical Science, University of Campinas - UNICAMP, São Paulo, Brazil.
Vanessa T GarridoINCT de Sangue, Hematology Center, School of Medical Science, University of Campinas - UNICAMP, São Paulo, Brazil.
Marina P ColellaINCT de Sangue, Hematology Center, School of Medical Science, University of Campinas - UNICAMP, São Paulo, Brazil.
Raquel SoaresDepartment of Biochemistry (I3S), Faculty of Medicine, University of Porto, Portugal.
Sara T Olalla-SaadINCT de Sangue, Hematology Center, School of Medical Science, University of Campinas - UNICAMP, São Paulo, Brazil.
Fernando F CostaINCT de Sangue, Hematology Center, School of Medical Science, University of Campinas - UNICAMP, São Paulo, Brazil.
Nicola ConranINCT de Sangue, Hematology Center, School of Medical Science, University of Campinas - UNICAMP, São Paulo, Brazil conran@unicamp.br.
Universidade Estadual de Campinas (UNICAMP) · BRUniversidade de São Paulo · BRUniversidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As hypoxia-induced inflammatory angiogenesis may contribute to the manifestations of sickle cell disease, we compared the angiogenic molecular profiles of plasma from sickle cell disease individuals and correlated these with in vitro endothelial cell-mediated angiogenesis-stimulating activity and in vivo neovascularization. Bioplex demonstrated that plasma from patients with steady-state sickle cell anemia contained elevated concentrations of pro-angiogenic factors (angiopoietin-1, basic fibroblast growth factor, vascular endothelial growth factor, vascular endothelial growth factor-D and placental growth factor) and displayed potent pro-angiogenic activity, significantly increasing endothelial cell proliferation, migration and capillary-like structure formation. In vivo neovascularization of Matrigel plugs was significantly greater in sickle cell disease mice than in non-sickle cell disease mice, consistent with an up-regulation of angiogenesis in the disease. In plasma from patients with hemoglobin SC disease without proliferative retinopathy, anti-angiogenic endostatin and thrombospondin-2 were significantly elevated. In contrast, plasma from hemoglobin SC individuals with proliferative retinopathy had a pro-angiogenic profile and more significant effects on endothelial cell proliferation and capillary formation than plasma from patients without retinopathy. Hydroxyurea therapy was associated with significant reductions in plasma angiogenic factors and inhibition of endothelial cell-mediated angiogenic mechanisms and neovascularization. Thus, individuals with sickle cell anemia or hemoglobin SC disease with retinopathy present a highly angiogenic circulating milieu, capable of stimulating key endothelial cell-mediated angiogenic mechanisms. Combination anti-angiogenic therapy to prevent the progression of unregulated neovascularization and associated manifestations in sickle cell disease, such as pulmonary hypertension, may be indicated; furthermore, the benefits and drawbacks of the potent anti-angiogenic effects of hydroxyurea should be clarified.

Indexed as

AdolescentAdultAnemia, Sickle CellAnimalsAntisickling AgentsEndothelial CellsFemaleHumansHuman Umbilical Vein Endothelial CellsHydroxyureaMaleMiceMice, Inbred C57BLMice, TransgenicMiddle AgedNeovascularization, PathologicAntisickling AgentsHydroxyurea

Identifiers

PMID25769545
PMCPMC4450618
OpenAlexW2075981185

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.