Evidence map›Paper›PMID 10074481›Full record

ArticleThe Journal of clinical investigation1999

P-selectin deficiency exacerbates experimental glomerulonephritis: a protective role for endothelial P-selectin in inflammation.

A R Rosenkranz, D L Mendrick, R S Cotran, T N Mayadas

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 122 citations in OpenAlex.

  1. Article
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  4. Article
  5. Re-Examining Neutrophil Participation in GN.Journal of the American Society of Nephrology : JASN · 2017
    Review
  6. Review
  7. Article
  8. Article
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  15. Article
  16. Article
  17. A murine model of phosphate nephropathy.The American journal of pathology · 2011
    Article
  18. Article
  19. 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

4 authors at 3 institutions in 1 country.

A R RosenkranzDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
D L Mendrick
R S Cotran
T N Mayadas
Brigham and Women's Hospital · USHarvard University · USHarvard University Press · US

Funding

AGBD T CELL DEPENDENT MECHANISMS OF GLOMERULONEPHRITISR01DK051643 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI MAYADAS, TANYA N. · 1996 to 2006
$1.3M
P-SELECTIN EXPRESSION AND LEUKOCYTE RECRUITMENT IN BRAINR01NS033296 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI MAYADAS, TANYA N. · 1994 to 1998
–
NIDDK NIH HHS DK-51643NIDDK NIH HHS R01 DK051643NINDS NIH HHS NS-33296
6 · The paper itself

Abstract

P-selectin is a leukocyte adhesion receptor present in endothelial cells and platelets. We examined the role of P-selectin in the autologous phase of an accelerated model of anti-glomerular basement membrane (GBM) glomerulonephritis using P-selectin-deficient mice and chimeric mice expressing P-selectin only in platelets or endothelial cells. P-selectin-deficient mice exhibited more severe glomerular damage with increased interstitial mononuclear leukocytic infiltrates, and had significantly increased proteinuria and mortality when compared to wild-type mice. P-selectin on the endothelium was predominantly responsible for protection from the exacerbated disease, because chimeric mice with endothelial P-selectin, and not mice with platelet P-selectin, showed glomerular injury similar to that in wild-type animals. Levels of soluble circulating P-selectin were increased in nephritic wild-type mice and in chimeric mice with endothelial P-selectin, but not platelet P-selectin. Levels of soluble P-selectin, which has been shown to be anti-inflammatory in vitro, were inversely associated with the severity of disease. P-selectin was not expressed in the endothelium of the glomerulus or interstitium. Thus, the protective effect in wild-type mice may be accounted for, in part by soluble P-selectin shed by non-renal endothelial cells, although other endothelial P-selectin-dependent mechanisms cannot be ruled out.

Indexed as

AnimalsAnti-Glomerular Basement Membrane DiseaseEndothelium, VascularImmunohistochemistryInflammationMiceMice, Inbred C57BLMice, KnockoutP-SelectinP-Selectin

Identifiers

PMID10074481
PMCPMC408121
OpenAlexW1974908144

What OpenQuestion holds

Texttitle and abstract
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.