Evidence map›Paper›PMID 32889753›Full record

ArticleJournal of cellular and molecular medicine2020

Transforming growth factor β-mediated micromechanics modulates disease progression in primary myelofibrosis.

Patric Teodorescu, Sergiu Pasca, Ancuta Jurj, Grigore Gafencu, Jon-Petur Joelsson, Sonia Selicean, Cristian Moldovan, Raluca Munteanu, Anca Onaciu, Adrian-Bogdan Tigu and 12 more

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
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  5. Article
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  8. DNA damage and repair in the hematopoietic system.Acta biochimica et biophysica Sinica · 2022
    Review
  9. Article
  10. Review
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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

22 authors.

Patric TeodorescuDepartment of Hematology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Sergiu PascaDepartment of Hematology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Ancuta JurjResearch Center for Functional Genomics and Translational Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Grigore GafencuResearch Center for Functional Genomics and Translational Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Jon-Petur JoelssonStem Cell Research Unit, Biomedical Center, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
Sonia SeliceanResearch Center for Functional Genomics and Translational Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Cristian MoldovanMedfuture Research Center for Advanced Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Raluca MunteanuMedfuture Research Center for Advanced Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Anca OnaciuMedfuture Research Center for Advanced Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Adrian-Bogdan TiguMedfuture Research Center for Advanced Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Mihail BuseMedfuture Research Center for Advanced Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Alina-Andreea ZimtaMedfuture Research Center for Advanced Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Rares StiufiucMedfuture Research Center for Advanced Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Bobe PetrushevMedfuture Research Center for Advanced Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Minodora DesmireanDepartment of Hematology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Delia DimaDepartment of Hematology, Ion Chiricuta Clinical Research Center, Cluj Napoca, Romania.
Cristina VladDepartment of Cardiology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Jon Thor BergthorssonStem Cell Research Unit, Biomedical Center, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
Cristian BerceAnimal Facility, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.
Stefan CiureaDepartment of Cellular Therapies and Stem Cell Transplantation, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Gabriel GhiaurDepartment of Leukemia, Sidney Kimmel Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-3955-7944
Ciprian TomuleasaDepartment of Hematology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj Napoca, Romania.ORCID 0000-0001-5500-1519

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary myelofibrosis (PMF) is a Ph-negative myeloproliferative neoplasm (MPN), characterized by advanced bone marrow fibrosis and extramedullary haematopoiesis. The bone marrow fibrosis results from excessive proliferation of fibroblasts that are influenced by several cytokines in the microenvironment, of which transforming growth factor-β (TGF-β) is the most important. Micromechanics related to the niche has not yet been elucidated. In this study, we hypothesized that mechanical stress modulates TGF-β signalling leading to further activation and subsequent proliferation and invasion of bone marrow fibroblasts, thus showing the important role of micromechanics in the development and progression of PMF, both in the bone marrow and in extramedullary sites. Using three PMF-derived fibroblast cell lines and transforming growth factor-β receptor (TGFBR) 1 and 2 knock-down PMF-derived fibroblasts, we showed that mechanical stress does stimulate the collagen synthesis by the fibroblasts in patients with myelofibrosis, through the TGFBR1, which however seems to be activated through alternative pathways, other than TGFBR2.

Indexed as

Disease ProgressionAnimalsBiomechanical PhenomenaFibroblastsHumansHypertension, PulmonaryMice, NudeModels, BiologicalPrimary MyelofibrosisReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IIStress, MechanicalTransforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IITransforming Growth Factor betafibroblast activationinvasionmicromechanicsmyelofibrosisproliferationTGF-β

Identifiers

PMID32889753
PMCPMC7576271

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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.