Evidence map›Paper›PMID 27256980›Full record

ArticleOncotarget2016

Dendritic cell-derived VEGF-A plays a role in inflammatory angiogenesis of human secondary lymphoid organs and is driven by the coordinated activation of multiple transcription factors.

Valentina Salvi, William Vermi, Veronica Gianello, Silvia Lonardi, Vincenzo Gagliostro, Antonella Naldini, Silvano Sozzani, Daniela Bosisio

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 39 citations in OpenAlex.

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  2. 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

8 authors at 2 institutions in 1 country.

Valentina SalviDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
William VermiDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Veronica GianelloDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Silvia LonardiDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Vincenzo GagliostroDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Antonella NaldiniDepartment of Molecular and Developmental Medicine, University of Siena, Siena, Italy.
Silvano SozzaniDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Daniela BosisioDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
University of Brescia · ITUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lymph node expansion during inflammation is essential to establish immune responses and relies on the development of blood and lymph vessels. Previous work in mice has shown that this process depends on the presence of VEGF-A produced by B cells, macrophages and stromal cells. In humans, however, the cell types and the mechanisms regulating the intranodal production of VEGF-A remain elusive. Here we show that CD11c+ cells represent the main VEGF-A-producing cell population in human reactive secondary lymphoid organs. In addition we find that three transcription factors, namely CREB, HIF-1α and STAT3, regulate the expression of VEGF-A in inflamed DCs. Both HIF-1α and STAT3 are activated by inflammatory agonists. Conversely, CREB phosphorylation represents the critical contribution of endogenous or exogenous PGE2. Taken together, these results propose a crucial role for DCs in lymph node inflammatory angiogenesis and identify novel potential cellular and molecular targets to limit inflammation in chronic diseases and tumors.

Indexed as

Neovascularization, PathologicAnimalsCD11c AntigenDendritic CellsDose-Response Relationship, DrugHumansHypoxia-Inducible Factor 1, alpha SubunitImmunoprecipitationInflammationLigandsLymph NodesMacrophagesMiceMonocytesMyeloid CellsPhosphorylationCD11c AntigenHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitLigandsPlatelet Endothelial Cell Adhesion Molecule-1STAT3 protein, humanSTAT3 Transcription FactorTranscription FactorsVascular Endothelial Growth Factor AVEGFA protein, humanCD1a+ interdigitating DCsCD1c+ DCsDAMPsdraining lymph nodePAMPsPathology Section

Identifiers

PMID27256980
PMCPMC5129930
OpenAlexW2412401448

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.