Evidence map›Paper›PMID 19176400›Full record

ArticleCancer research2009

Signal transducers and activators of transcription mediate fibroblast growth factor-induced vascular endothelial morphogenesis.

Xinhai Yang, Dianhua Qiao, Kristy Meyer, Andreas Friedl

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 68 citations in OpenAlex.

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  6. FGF Signaling Directs the Cell Fate Switch from Neurons to Astrocytes in the Developing Mouse Cerebral Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
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  11. Decreased expression of RPS15A suppresses proliferation of lung cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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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

4 authors at 1 institution in 1 country.

Xinhai YangDepartment of Pathology, Laboratory Medicine, University of Wisconsin-Madison, Madison, Wisconsin 53792, USA.
Dianhua Qiao
Kristy Meyer
Andreas Friedl
University of Wisconsin–Madison · US

Funding

Heparan Sulfate Proteoglycans in Glioma AngiogenesisR01NS048921 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI FRIEDL, ANDREAS · 2004 to 2008
$1.3M
NINDS NIH HHS R01 NS048921NINDS NIH HHS R01 NS048921-01
6 · The paper itself

Abstract

The fibroblast growth factors (FGF) play diverse roles in development, wound healing, and angiogenesis. The intracellular signal transduction pathways, which mediate these pleiotropic activities, remain incompletely understood. We show here that the proangiogenic factors FGF2 and FGF8b can activate signal transducers and activators of transcription (STAT) in mouse microvascular endothelial cells (EC). Both FGF2 and FGF8b activate STAT5 and to a lesser extent STAT1, but not STAT3. The FGF2-dependent activation of endothelial STAT5 was confirmed in vivo with the Matrigel plug angiogenesis assay. In tissue samples of human gliomas, a tumor type wherein FGF-induced angiogenesis is important, STAT5 is detected in tumor vessel EC nuclei, consistent with STAT5 activation. By forced expression of constitutively active or dominant-negative mutant STAT5A in mouse brain ECs, we further show that STAT5 activation is both necessary and sufficient for FGF-induced cell migration, invasion, and tube formation, which are key events in vascular endothelial morphogenesis and angiogenesis. In contrast, STAT5 is not required for brain EC mitogenesis. The cytoplasmic tyrosine kinases Src and Janus kinase 2 (Jak2) both seem to be involved in the activation of STAT5, as their inhibition reduces FGF2- and FGF8b-induced STAT5 phosphorylation and EC tube formation. Constitutively active STAT5A partially restores tube formation in the presence of Src or Jak2 inhibitors. These observations show that FGFs use distinct signaling pathways to induce angiogenic phenotypes. Together, our findings implicate the FGF-Jak2/Src-STAT5 cascade as a critical angiogenic FGF signaling pathway.

Indexed as

AdenoviridaeAnimalsBrainCell NucleusEndothelium, VascularFibroblast Growth FactorsMiceMicrocirculationMorphogenesisNeovascularization, PhysiologicPlasmidsSignal TransductionSTAT5 Transcription FactorWound HealingFibroblast Growth FactorsStat5a protein, mouseSTAT5 Transcription Factor

Identifiers

PMID19176400
PMCPMC2650265
OpenAlexW2134885863

What OpenQuestion holds

Textmetadata
LicenceTDM
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.