Evidence map›Paper›PMID 22267482›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Long pentraxin 3/tumor necrosis factor-stimulated gene-6 interaction: a biological rheostat for fibroblast growth factor 2-mediated angiogenesis.

Daria Leali, Antonio Inforzato, Roberto Ronca, Roberta Bianchi, Mirella Belleri, Daniela Coltrini, Emanuela Di Salle, Marina Sironi, Giuseppe Danilo Norata, Barbara Bottazzi and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.2field-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

37 citing papers in PubMed, 74 citations in OpenAlex.

  1. Modulation of diabetes-related retinal pathophysiology by PTX3.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  5. Role of long pentraxin PTX3 in cancer.Clinical and experimental medicine · 2023
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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

13 authors at 2 institutions in 1 country.

Daria LealiDepartment of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia, Viale Europa 11, 25123 Brescia, Italy.
Antonio Inforzato
Roberto Ronca
Roberta Bianchi
Mirella Belleri
Daniela Coltrini
Emanuela Di Salle
Marina Sironi
Giuseppe Danilo Norata
Barbara Bottazzi
Cecilia Garlanda
Anthony J Day
Marco Presta
Istituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Milan · IT

Funding

Arthritis Research UK 16539Arthritis Research UK 18472Medical Research Council G0701180Medical Research Council G0701180(84646)
6 · The paper itself

Abstract

objectiveAngiogenesis is regulated by the balance between pro- and antiangiogenic factors and by extracellular matrix protein interactions. Fibroblast growth factor 2 (FGF2) is a major proangiogenic inducer inhibited by the interaction with the soluble pattern recognition receptor long pentraxin 3 (PTX3). PTX3 is locally coexpressed with its ligand tumor necrosis factor-stimulated gene-6 (TSG-6), a secreted glycoprotein that cooperates with PTX3 in extracellular matrix assembly. Here, we characterized the effect of TSG-6 on PTX3/FGF2 interaction and FGF2-mediated angiogenesis. METHODS AND

resultsSolid phase binding and surface plasmon resonance assays show that TSG-6 and FGF2 bind the PTX3 N-terminal domain with similar affinity. Accordingly, TSG-6 prevents FGF2/PTX3 interaction and suppresses the inhibition exerted by PTX3 on heparan sulfate proteoglycan/FGF2/FGF receptor complex formation and on FGF2-dependent angiogenesis in vitro and in vivo. Also, endogenous PTX3 exerts an inhibitory effect on vascularization induced by FGF2 in a murine subcutaneous Matrigel plug assay, the inhibition being abolished in Ptx3-null mice or by TSG-6 treatment in wild-type animals.

conclusionTSG-6 reverts the inhibitory effects exerted by PTX3 on FGF2-mediated angiogenesis through competition of FGF2/PTX3 interaction. This may provide a novel mechanism to control angiogenesis in those pathological settings characterized by the coexpression of TSG-6 and PTX3, in which the relative levels of these proteins may fine-tune the angiogenic activity of FGF2.

Indexed as

Neovascularization, PhysiologicAnimalsBinding, CompetitiveCattleCell Adhesion MoleculesChick EmbryoCHO CellsC-Reactive ProteinCricetinaeCricetulusFemaleFibroblast Growth Factor 2HEK293 CellsHeparan Sulfate ProteoglycansHumansMiceCell Adhesion MoleculesC-Reactive ProteinFibroblast Growth Factor 2Heparan Sulfate ProteoglycansNerve Tissue ProteinsPentraxinsRecombinant ProteinsSerum Amyloid P-ComponentTNFAIP6 protein, human

Identifiers

PMID22267482
PMCPMC3551298
OpenAlexW2529490970

What OpenQuestion holds

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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.