Evidence map›Paper›PMID 11159195›Full record

ArticleThe American journal of pathology2001

Internalization of proteinase 3 is concomitant with endothelial cell apoptosis and internalization of myeloperoxidase with generation of intracellular oxidants.

J J Yang, G A Preston, W F Pendergraft, M Segelmark, P Heeringa, S L Hogan, J C Jennette, R J Falk

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Characterization of Myeloperoxidase in the Healthy Equine Endometrium.Animals : an open access journal from MDPI · 2023
    Article
  12. Article
  13. Mechanisms of vascular damage in ANCA vasculitis.Seminars in immunopathology · 2022
    Review
  14. Review
  15. Review
  16. Autoantibody Biomarkers in Rheumatic Diseases.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Article
  19. Identification of Tengfu Jiangya Tablet Target Biomarkers with Quantitative Proteomic Technique.Evidence-based complementary and alternative medicine : eCAM · 2017
    Article
  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

8 authors at 3 institutions in 2 countries.

J J YangDepartment of Medicine and Hypertension, Division of Nephrology and Hypertension, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7155, USA. jjyang@med.unc.edu
G A Preston
W F Pendergraft
M Segelmark
P Heeringa
S L Hogan
J C Jennette
R J Falk
University of North Carolina at Chapel Hill · USHypertension Institute · USLund University · SE

Funding

NEUTROPHIL AUTOANTIBODIES IN VASCULITIS AND NEPHRITISR01DK040208 · NIDDK · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI FALK, RONALD J · 1989 to 2000
$231k
NIDDK NIH HHS DK 40208
6 · The paper itself

Abstract

The important issue addressed by the studies presented here is the mechanism of neutrophil-mediated damage to endothelial and epithelial cells during inflammation. Binding of neutrophil-released granule proteins to endothelial cells may be involved in vascular damage in patients with inflammatory vascular diseases. We have determined whether granule proteins proteinase 3(PR3) and/or myeloperoxidase (MPO) are internalized into endothelial cells, as examined by UV light, confocal, and electron microscopy. Coincident induction of apoptosis and/or the generation of intracellular oxidants were monitored. The results indicate that human endothelial cells (human umbilical vein endothelial cells, human umbilical arterial endothelial cells, human lung microvascular endothelial cells) internalize both PR3 and MPO, which are detected on the cell surface, in the cytoplasm, and possibly nuclear. Epithelial cells (small airway epithelial cells) internalized MPO but not PR3, implying that the mechanism of PR3 internalization may be cell-type specific and different from that of MPO. Internalization of PR3, but not MPO, correlated with activation of apoptosis. Internalization of MPO correlated with an increase in intracellular oxidant radicals. The requirement for the proteolytic activity of PR3 for the induction of apoptosis was examined by generating PR3-truncated fragments that did not contain the components of the catalytic triad. An apoptotic function was localized to the C-terminal portion of PR3. These studies reveal novel mechanisms by which the neutrophil granule proteins PR3 and MPO contribute to tissue injury at sites of inflammation.

Indexed as

ApoptosisBiological TransportCells, CulturedEndocytosisEndothelium, VascularHumansMicroscopy, ElectronMicroscopy, FluorescenceMyeloblastinOxidantsOxidation-ReductionPeroxidaseProtein Structure, TertiarySerine EndopeptidasesTime FactorsMyeloblastinOxidantsPeroxidaseSerine Endopeptidases

Identifiers

PMID11159195
PMCPMC1850298
OpenAlexW2085575421

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.