Evidence map›Paper›PMID 18566344›Full record

ArticleCirculation research2008

Neurotrophin p75 receptor (p75NTR) promotes endothelial cell apoptosis and inhibits angiogenesis: implications for diabetes-induced impaired neovascularization in ischemic limb muscles.

Andrea Caporali, Elisabetta Pani, Anton J G Horrevoets, Nicolle Kraenkel, Atsuhiko Oikawa, Graciela B Sala-Newby, Marco Meloni, Brunella Cristofaro, Gallia Graiani, Aurelie S Leroyer and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

54 citing papers in PubMed, 98 citations in OpenAlex.

  1. Trial
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  10. Review
  11. In vivo functions of p75Trends in pharmacological sciences · 2021
    Review
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  18. Deletion of p75Scientific reports · 2018
    Article
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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

15 authors at 3 institutions in 2 countries.

Andrea CaporaliExperimental Cardiovascular Medicine Division, Bristol Heart Institute, University of Bristol, UK.
Elisabetta Pani
Anton J G Horrevoets
Nicolle Kraenkel
Atsuhiko Oikawa
Graciela B Sala-Newby
Marco Meloni
Brunella Cristofaro
Gallia Graiani
Aurelie S Leroyer
Chantal M Boulanger
Gaia Spinetti
Sung Ok Yoon
Paolo Madeddu
Costanza Emanueli
MultiMedica · ITUniversity of Parma · ITAmsterdam UMC Location VUmc · NL

Funding

Crosstalk between NGS Receptors, TrkA &P75R01NS039472 · NINDS · OHIO STATE UNIVERSITY · PI YOON, SUNG OK · 2000 to 2009
$3.0M
British Heart Foundation RJ4430British Heart Foundation RJ4769British Heart Foundation SM6266NINDS NIH HHS R01 NS039472
6 · The paper itself

Abstract

Diabetes impairs endothelial function and reparative neovascularization. The p75 receptor of neurotrophins (p75(NTR)), which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice. Here, we show that gene transfer-induced p75(NTR) expression impairs the survival, proliferation, migration, and adhesion capacities of cultured ECs and endothelial progenitor cells (EPCs) and inhibits angiogenesis in vitro. Moreover, intramuscular p75(NTR) gene delivery impairs neovascularization and blood flow recovery in a mouse model of limb ischemia. These disturbed functions are associated with suppression of signaling mechanisms implicated in EC survival and angiogenesis. In fact, p75(NTR) depresses the VEGF-A/Akt/eNOS/NO pathway and additionally reduces the mRNA levels of ITGB1 [beta (1) integrin], BIRC5 (survivin), PTTG1 (securin) and VEZF1. Diabetic mice, which typically show impaired postischemic muscular neovascularization and blood perfusion recovery, have these defects corrected by intramuscular gene transfer of a dominant negative mutant form of p75(NTR). Collectively, our data newly demonstrate the antiangiogenic action of p75(NTR) and open new avenues for the therapeutic use of p75(NTR) inhibition to combat diabetes-induced microvascular liabilities.

Indexed as

AnimalsApoptosisCells, CulturedDiabetes Mellitus, ExperimentalDiabetic AngiopathiesDisease Models, AnimalEndothelium, VascularHumansIschemiaMaleMiceMice, Inbred StrainsMuscle, SkeletalNeovascularization, PhysiologicNitric OxideNitric Oxide SynthaseNitric OxideNitric Oxide SynthaseProto-Oncogene Proteins c-aktReceptor, Nerve Growth FactorStreptozocinVascular Endothelial Growth Factor A

Identifiers

PMID18566344
PMCPMC2640941
OpenAlexW2134183266

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.