Evidence map›Paper›PMID 23998130›Full record

ArticleJournal of diabetes research2013

Pronerve growth factor induces angiogenesis via activation of TrkA: possible role in proliferative diabetic retinopathy.

Sally L Elshaer, Mohammed A Abdelsaid, Ahmad Al-Azayzih, Parag Kumar, Suraporn Matragoon, Julian J Nussbaum, Azza B El-Remessy

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. The innate immune system in diabetic retinopathy.Progress in retinal and eye research · 2021
    Review
  3. Modulation of p75International journal of molecular sciences · 2021
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Deletion of p75Scientific reports · 2018
    Article
  9. Implication of the neurotrophin receptor p75Expert review of ophthalmology · 2017
    Article
  10. Deletion of the Neurotrophin Receptor p75Journal of diabetes, metabolic disorders & control · 2017
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. 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

7 authors at 2 institutions in 1 country.

Sally L ElshaerCenter for Pharmacy and Experimental Therapeutics, University of Georgia, 1120 15th Street HM-1200, Augusta, GA 30912, USA.
Mohammed A Abdelsaid
Ahmad Al-Azayzih
Parag Kumar
Suraporn Matragoon
Julian J Nussbaum
Azza B El-Remessy
University of Georgia · USDiscovery Institute · US

Funding

Molecular Mechanisms of diabetic retinopathyR01EY022408 · NEI · UNIVERSITY OF GEORGIA · PI EL-REMESSY, AZZA B · 2012 to 2016
$1.5M
NEI NIH HHS R01 EY022408NEI NIH HHS R0-1EY-022408
6 · The paper itself

Abstract

Proliferative diabetic retinopathy (PDR) is the leading cause of blindness in working age Americans. We demonstrated that diabetes disturbs the homeostasis of nerve growth factor (NGF) resulting in accumulation of its precursor proNGF. Increases in proNGF were positively correlated with progression of diabetic retinopathy, having the highest level in ocular fluids from PDR patients compared to nondiabetic patients. Here, we attempted to evaluate the contribution and the possible mechanism of proNGF to PDR. The angiogenic response of aqueous humor samples from PDR patients was examined in human retinal endothelial cells in the presence or absence of anti-proNGF antibody. Additional cultures were treated with mutant-proNGF in the presence of specific pharmacological inhibitors of TrkA and p75(NTR) receptors. PDR-aqueous humor samples exerted significant angiogenic response including cell proliferation, migration, and alignment into tube-like structures. These effects were significantly reduced by anti-proNGF antibody but not by IgG. Treatment of retinal endothelial cells with mutant-proNGF activated phosphorylation of TrkA and p38MAPK; however, it did not alter p75(NTR) expression. Inhibition of TrkA but not p75(NTR) significantly reduced mutant-proNGF-induced cell proliferation, cell migration, and tube formation. Taken together, these results provide evidence that proNGF can contribute to PDR at least in part via activation of TrkA.

Indexed as

AdolescentAdultAqueous HumorCell MovementCell ProliferationDiabetic RetinopathyEndothelial CellsFemaleHumansMaleNeovascularization, PathologicNerve Growth Factorp38 Mitogen-Activated Protein KinasesPhosphorylationProtein PrecursorsReceptor, trkANerve Growth Factorp38 Mitogen-Activated Protein Kinasespro-nerve growth factor, humanProtein PrecursorsReceptor, trkA

Identifiers

PMID23998130
PMCPMC3753742
OpenAlexW2139364735

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.