Evidence map›Paper›PMID 11021829›Full record

ArticleThe American journal of pathology2000

p75(NTR) mediates neurotrophin-induced apoptosis of vascular smooth muscle cells.

S Wang, P Bray, T McCaffrey, K March, B L Hempstead, R Kraemer

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. [Research progress of P75 neurotrophin receptor and new idea of nonunion treatment].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2017
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Brain-derived neurotrophic factor in the airways.Pharmacology & therapeutics · 2014
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Neurotrophins in lung health and disease.Expert review of respiratory medicine · 2010
    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 at 2 institutions in 1 country.

S WangDepartments of Pathology and Medicine, Joan and Sanford I. Weill Medical College of Cornell University, New York, New York, USA.
P Bray
T McCaffrey
K March
B L Hempstead
R Kraemer
Cornell University · USRichard L. Roudebush VA Medical Center · US

Funding

Vascular signaling via scavenger receptorsP01HL046403 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI HAJJAR, KATHERINE AMBERSON · 1991 to 2011
$26.7M
SCOR IN MOLECULAR MEDICINE AND ATHEROSCLEROSISP50HL056987 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI CRYSTAL, RONALD G · 1997 to 2001
$2.4M
P75NTR and Apoptosis of Neointimal Smooth Muscle CellsR01HL058623 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI KRAEMER, ROSEMARY · 1997 to 2004
$1.4M
NHLBI NIH HHS HL56987NHLBI NIH HHS HL 58623NHLBI NIH HHS P01 HL046403NHLBI NIH HHS P01HL46403NHLBI NIH HHS R01 HL058623
6 · The paper itself

Abstract

The development of atherosclerotic lesions results from aberrant cell migration, proliferation, and extracellular matrix production. In advanced lesions, however, cellular apoptosis, leading to lesion remodeling, predominates. During lesion formation, the neurotrophins and the neurotrophin receptor tyrosine kinases, trks B and C, are induced and mediate smooth muscle cell migration. Here we demonstrate that a second neurotrophin receptor, p75(NTR), is expressed by established human atherosclerotic lesions and late lesions that develop after balloon injury of the rat thoracic aorta. The p75(NTR), a member of the tumor necrosis factor/FAS receptor family, can modulate trk receptor function as well as initiate cell death when expressed in cells of the nervous system that lack kinase-active trk receptors. p75(NTR) expression colocalizes to neointimal cells, which express smooth muscle cell alpha-actin and are expressed by cultured human endarterectomy-derived cells (HEDC). Areas of the plaque expressing p75(NTR) demonstrate increased TUNEL positivity, and HEDC undergo apoptosis in response to the neurotrophins. Finally, neurotrophins also induced apoptosis of a smooth muscle cell line genetically manipulated to express p75(NTR), but lacking trk receptor expression. These studies identify the regulated expression of neurotrophins and p75(NTR) as an inducer of smooth muscle cell apoptosis in atherosclerotic lesions.

Indexed as

AnimalsApoptosisArteriosclerosisCells, CulturedHumansIn Situ Nick-End LabelingMaleMiceMuscle, Smooth, VascularNerve Growth FactorsPolysaccharidesRatsRats, Sprague-DawleyReceptor, Nerve Growth FactorTemperatureTissue DistributionNerve Growth FactorsneurotropinPolysaccharidesReceptor, Nerve Growth Factor

Identifiers

PMID11021829
PMCPMC1850174
OpenAlexW2043188646

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.