Evidence map›Paper›PMID 20360537›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2010

Neurotrophin-3 is a novel angiogenic factor capable of therapeutic neovascularization in a mouse model of limb ischemia.

Brunella Cristofaro, Oliver A Stone, Andrea Caporali, David Dawbarn, Nicholas Ieronimakis, Morayma Reyes, Paolo Madeddu, David O Bates, Costanza Emanueli

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
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  11. Nervous System-Driven Osseointegration.International journal of molecular sciences · 2022
    Review
  12. Review
  13. Article
  14. Innervation in organogenesis.Current topics in developmental biology · 2022
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Depression and Cardiovascular Disease: The Viewpoint of Platelets.International journal of molecular sciences · 2020
    Review
  20. Article
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

9 authors at 1 institution in 2 countries.

Brunella CristofaroExperimental Cardiovascular Medicine Division, University of Bristol, Bristol, England, UK.
Oliver A Stone
Andrea Caporali
David Dawbarn
Nicholas Ieronimakis
Morayma Reyes
Paolo Madeddu
David O Bates
Costanza Emanueli
University of Washington · US

Funding

British Heart Foundation BS/05/001/18360British Heart Foundation RJ4430
6 · The paper itself

Abstract

objectiveTo investigate the novel hypothesis that neurotrophin-3 (NT-3), an established neurotrophic factor that participates in embryonic heart development, promotes blood vessel growth. METHODS AND

resultsWe evaluated the proangiogenic capacity of recombinant NT-3 in vitro and of NT-3 gene transfer in vivo (rat mesenteric angiogenesis assay and mouse normoperfused adductor muscle). Then, we studied whether either transgenic or endogenous NT-3 mediates postischemic neovascularization in a mouse model of limb ischemia. In vitro, NT-3 stimulated endothelial cell survival, proliferation, migration, and network formation on the basement membrane matrix Matrigel. In the mesenteric assay, NT-3 increased the number and size of functional vessels, including vessels covered with mural cells. Consistently, NT-3 overexpression increased muscular capillary and arteriolar densities in either the absence or the presence of ischemia and improved postischemic blood flow recovery in mouse hind limbs. NT-3-induced microvascular responses were accompanied by tropomyosin receptor kinase C (an NT-3 high-affinity receptor) phosphorylation and involved the phosphatidylinositol 3-kinase-Akt kinase-endothelial nitric oxide synthase pathway. Finally, endogenous NT-3 was shown to be essential in native postischemic neovascularization, as demonstrated by using a soluble tropomyosin receptor kinase C receptor domain that neutralizes NT-3.

conclusionsOur results provide the first insight into the proangiogenic capacity of NT-3 and propose NT-3 as a novel potential agent for the treatment of ischemic disease.

Indexed as

Genetic TherapyNeovascularization, PhysiologicAngiogenic ProteinsAnimalsCell MovementCell ProliferationCells, CulturedCell SurvivalDisease Models, AnimalEndothelial CellsHindlimbHumansIschemiaMaleMesenteryMiceAngiogenic ProteinsNerve Growth FactorsNeurotrophin 3neurotropin 3, mouseNitric Oxide Synthase Type IIINos3 protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, trkCRecombinant ProteinsRNA, Messenger

Identifiers

PMID20360537
PMCPMC2881585
OpenAlexW1998096648

What OpenQuestion holds

Textmetadata
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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.