Evidence map›Paper›PMID 18624773›Full record

ArticleJournal of cellular and molecular medicine2009

A pro-inflammatory signature mediates FGF2-induced angiogenesis.

Germán Andrés, Daria Leali, Stefania Mitola, Daniela Coltrini, Maura Camozzi, Michela Corsini, Mirella Belleri, Emilio Hirsch, Reto A Schwendener, Gerhard Christofori and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2009. 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
0.8field-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

37 citing papers in PubMed, 69 citations in OpenAlex.

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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

12 authors at 5 institutions in 3 countries.

Germán AndrésUnit of General Pathology and Immunology, Department of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia, Brescia, Italy.
Daria LealiUnit of General Pathology and Immunology, Department of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia, Brescia, Italy.
Stefania MitolaUnit of General Pathology and Immunology, Department of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia, Brescia, Italy.
Daniela ColtriniUnit of General Pathology and Immunology, Department of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia, Brescia, Italy.
Maura CamozziUnit of General Pathology and Immunology, Department of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia, Brescia, Italy.
Michela CorsiniUnit of General Pathology and Immunology, Department of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia, Brescia, Italy.
Mirella BelleriUnit of General Pathology and Immunology, Department of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia, Brescia, Italy.
Emilio HirschDepartment of Genetics, Biology and Biochemistry, University of Turin, Turin, Italy.
Reto A SchwendenerLaboratory of Liposome Research, Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
Gerhard ChristoforiInstitute of Biochemistry and Genetics, Department of Clinical Biological Sciences, University of Basel, Basel, Switzerland.
Antonio AlcamìCentro de Biologìa Molecular Severo Ochoa (CSIC-UAM), Campus Universidad Autónoma, Cantoblanco, Madrid, Spain.
Marco PrestaUnit of General Pathology and Immunology, Department of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia, Brescia, Italy.
University of Brescia · ITCentro de Biología Molecular Severo Ochoa · ESUniversity of Basel · CHUniversity of Turin · ITUniversity of Zurich · CH

Funding

Wellcome Trust
6 · The paper itself

Abstract

Fibroblast growth factor-2 (FGF2) is a potent angiogenic growth factor. Here, gene expression profiling of FGF2-stimulated microvascular endothelial cells revealed, together with a prominent pro-angiogenic profile, a pro-inflammatory signature characterized by the upregulation of pro-inflammatory cytokine/chemokines and their receptors, endothelial cell adhesion molecules and members of the eicosanoid pathway. Real-time quantitative PCR demonstrated early induction of most of the FGF2-induced, inflammation-related genes. Accordingly, chick embryo chorioallantoic membrane (CAM) and murine Matrigel plug angiogenesis assays demonstrated a significant monocyte/macrophage infiltrate in the areas of FGF2-driven neovascularization. Similar results were obtained when the conditioned medium (CM) of FGF2-stimulated endothelial cells was delivered onto the CAM, suggesting that FGF2-upregulated chemoattractants mediate the inflammatory response. Importantly, FGF2-triggered new blood vessel formation was significantly reduced in phosphatidylinositol 3-kinase-gamma null mice exhibiting defective leucocyte migration or in clodronate liposome-treated, macrophage-depleted mice. Furthermore, the viral pan-chemokine antagonist M3 inhibited the angiogenic and inflammatory responses induced by the CM of FGF2-stimulated endothelial cells and impaired FGF2-driven neovascularization in the CAM assay. These findings point to inflammatory chemokines as early mediators of FGF2-driven angiogenesis and indicate a non-redundant role for inflammatory cells in the neovascularization process elicited by the growth factor.

Indexed as

AnimalsBase SequenceChick EmbryoDNA PrimersFibroblast Growth Factor 2HumansMiceMice, Inbred C57BLMice, KnockoutNeovascularization, PhysiologicPhosphatidylinositol 3-KinasesPolymerase Chain ReactionRecombinant ProteinsDNA PrimersFibroblast Growth Factor 2Phosphatidylinositol 3-KinasesRecombinant Proteins

Identifiers

PMID18624773
PMCPMC6512373
OpenAlexW2085939323

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.