Evidence map›Paper›PMID 24848261›Full record

ArticlePloS one2014

FGF21 promotes endothelial cell angiogenesis through a dynamin-2 and Rab5 dependent pathway.

Usman Yaqoob, Kumaravelu Jagavelu, Uday Shergill, Thiago de Assuncao, Sheng Cao, Vijay H Shah

Abstract read
In one paragraph

Article in PloS one, 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
–field-weighted citation impact
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.

  1. Review
  2. Article
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  14. Fibroblast growth factors in cardiovascular disease: The emerging role of FGF21.American journal of physiology. Heart and circulatory physiology · 2015
    Review
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

6 authors.

Usman YaqoobGastroenterology Research Unit, Mayo Clinic, Rochester, Minnesota, United States of America.
Kumaravelu JagaveluGastroenterology Research Unit, Mayo Clinic, Rochester, Minnesota, United States of America.
Uday ShergillGastroenterology Research Unit, Mayo Clinic, Rochester, Minnesota, United States of America.
Thiago de AssuncaoGastroenterology Research Unit, Mayo Clinic, Rochester, Minnesota, United States of America.
Sheng CaoGastroenterology Research Unit, Mayo Clinic, Rochester, Minnesota, United States of America.
Vijay H ShahGastroenterology Research Unit, Mayo Clinic, Rochester, Minnesota, United States of America.

Funding

PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI Nicholas F. LaRusso · 2009 to 2026
$22.2M
Molecular Mechanisms of Portal HypertensionR01DK059615 · NIDDK · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H. · 2002 to 2023
$6.4M
Molecular Mechanisms of Portal HypertensionR56DK059615 · NIDDK · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H · 2007 to 2007
$378k
NIDDK NIH HHS DK084567NIDDK NIH HHS DK59615NIDDK NIH HHS P30 DK084567NIDDK NIH HHS R01 DK059615NIDDK NIH HHS R56 DK059615
6 · The paper itself

Abstract

Binding of angiogenic molecules with cognate receptor tyrosine kinases (RTK) is required for angiogenesis however the precise link between RTK binding, endocytosis, and signaling requires further investigation. Here, we use FGFR1 as a model to test the effects of the large GTPase and endocytosis regulatory molecule dynamin-2 on angiogenic signaling in context of distinct FGF ligands. In vitro, overexpression of dominant negative dynamin-2 (DynK44A) attenuates FGFR1 activation of Erk and tubulogenesis by FGF2. Furthermore, we identify FGF21, a non-classical, FGF ligand implicated in diverse human pathologies as an angiogenic molecule acting through FGFR1 and β-Klotho coreceptor. Disruption of FGFR1 activation of ERK by FGF21 is achieved by perturbation of the function of both dynamin-2 and Rab5 GTPase. In vivo, mice harboring endothelial selective overexpression of DynK44A, show impaired angiogenesis in response to FGF21. In conclusion, dynamin dependent endocytosis of FGFR1 is required for in vitro and in vivo angiogenesis in response to FGF2 and the non-classical FGF ligand, FGF21. These studies extend our understanding of the relationships between RTK binding, internalization, endosomal targeting, and angiogenic signaling.

Indexed as

Gene Expression RegulationNeovascularization, PathologicAnimalsDynamin IIEndocytosisEndosomesEndothelial CellsFibroblast Growth Factor 2Fibroblast Growth FactorsHumansHuman Umbilical Vein Endothelial CellsKlotho ProteinsLigandsLiver CirrhosisMaleMembrane ProteinsDynamin IIFibroblast Growth Factor 2fibroblast growth factor 21Fibroblast Growth FactorsKLB protein, humanKlb protein, mouseKlotho ProteinsLigandsMembrane ProteinsRAB5C protein, humanrab5 GTP-Binding Proteins

Identifiers

PMID24848261
PMCPMC4029959

What OpenQuestion holds

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LicenceCC BY
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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.