Evidence map›Paper›PMID 24450584›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

Nuclear localization of vascular endothelial growth factor-D and regulation of c-Myc-dependent transcripts in human lung fibroblasts.

Souheil El-Chemaly, Gustavo Pacheco-Rodriguez, Daniela Malide, Victor Meza-Carmen, Jiro Kato, Ye Cui, Philip I Padilla, Arun Samidurai, Bernadette R Gochuico, Joel Moss

Open access · greenAbstract readComparative Study
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  4. Article
  5. CBClinical and translational medicine · 2021
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  6. Review
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  13. Pulmonary Vasculopathy Associated with FIGF Gene Mutation.The American journal of pathology · 2017
    Article
  14. 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

10 authors at 3 institutions in 1 country.

Souheil El-Chemaly1 From the Cardiovascular and Pulmonary Branch.
Gustavo Pacheco-Rodriguez
Daniela Malide
Victor Meza-Carmen
Jiro Kato
Ye Cui
Philip I Padilla
Arun Samidurai
Bernadette R Gochuico
Joel Moss
Brigham and Women's Hospital · USNational Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Characterization of the Pathogenesis of Lymphangioleiomyomatosis (LAM)ZIAHL002541 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MOSS, JOEL · 2009 to 2025
$47.7M
Light Microscopy CoreZICHL006019 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI COMBS, CHRISTIAN · 2009 to 2025
$29.3M
Intracellular Actions of the Lymphangiogenic Growth Factor VEGF-D in FibroblastsK22HL092223 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI EL-CHEMALY, SOUHEIL · 2012 to 2013
$324k
Intramural NIH HHSNHLBI NIH HHS 1K22HL092223NHLBI NIH HHS K22 HL092223
6 · The paper itself

Abstract

Lymphangiogenesis and angiogenesis are processes that are, in part, regulated by vascular endothelial growth factor (VEGF)-D. The formation of lymphatic structures has been implicated in multiple lung diseases, including pulmonary fibrosis. VEGF-D is a secreted protein produced by fibroblasts and macrophages, which induces lymphangiogenesis by signaling via VEGF receptor-3, and angiogenesis through VEGF receptor-2. VEGF-D contains a central VEGF homology domain, which is the biologically active domain, with flanking N- and C-terminal propeptides. Full-length VEGF-D (∼ 50 kD) is proteolytically processed in the extracellular space, to generate VEGF homology domain that contains the VEGF-D receptor-binding sites. Here, we report that, independent of its cell surface receptors, full-length VEGF-D accumulated in nuclei of fibroblasts, and that this process appears to increase with cell density. In nuclei, full-length VEGF-D associated with RNA polymerase II and c-Myc. In cells depleted of VEGF-D, the transcriptionally regulated genes appear to be modulated by c-Myc. These findings have potential clinical implications, as VEGF-D was found in fibroblast nuclei in idiopathic pulmonary fibrosis, a disease characterized by fibroblast proliferation. These findings are consistent with actions of full-length VEGF-D in cellular homeostasis in health and disease, independent of its receptors.

Indexed as

Gene Expression ProfilingGene Expression RegulationBiomarkersBlotting, WesternCell NucleusCell ProliferationCells, CulturedFibroblastsHumansIdiopathic Pulmonary FibrosisImmunoprecipitationOligonucleotide Array Sequence AnalysisProto-Oncogene Proteins c-mycSignal TransductionVascular Endothelial Growth Factor DVascular Endothelial Growth Factor Receptor-2BiomarkersMYC protein, humanProto-Oncogene Proteins c-mycVascular Endothelial Growth Factor DVascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth Factor Receptor-3VEGFD protein, humanc-Mycfibroblastidiopathic pulmonary fibrosisnucleivascular endothelial growth factor-D

Identifiers

PMID24450584
PMCPMC4091860
OpenAlexW2065835329

What OpenQuestion holds

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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.