Evidence map›Paper›PMID 8083378›Full record

ArticleThe Journal of clinical investigation1994

Fibrinogen mediates platelet-polymorphonuclear leukocyte cooperation during immune-complex glomerulonephritis in rats.

X Wu, M H Helfrich, M A Horton, L P Feigen, J B Lefkowith

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1994. 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
1.2field-weighted citation impact, top 21% 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, 44 citations in OpenAlex.

  1. Article
  2. Inflammogenesis of Secondary Spinal Cord Injury.Frontiers in cellular neuroscience · 2016
    Review
  3. Update on crescentic glomerulonephritis.Seminars in immunopathology · 2014
    Review
  4. Article
  5. Review
  6. Neutrophils: game changers in glomerulonephritis?Trends in molecular medicine · 2010
    Review
  7. TLR4 links podocytes with the innate immune system to mediate glomerular injury.Journal of the American Society of Nephrology : JASN · 2008
    Article
  8. Leukocytes in glomerular injury.Seminars in immunopathology · 2007
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Role of platelets in progressive glomerular diseases.Pediatric nephrology (Berlin, Germany) · 1995
    Review
  14. Article
  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

5 authors at 2 institutions in 2 countries.

X WuDepartment of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.
M H Helfrich
M A Horton
L P Feigen
J B Lefkowith
Washington University in St. Louis · USSt Bartholomew's Hospital · GB

Funding

ROLE OF ESSENTIAL FATTY ACID IN GLOMERULONEPHRITISR01DK037879 · NIDDK · WASHINGTON UNIVERSITY · PI LEFKOWITH, JAMES B · 1987 to 1994
–
NIDDK NIH HHS DK-37879
6 · The paper itself

Abstract

The metabolic and functional alterations which occur during the acute phase of nephrotoxic nephritis (NTN) in rats, a model of immune-mediated glomerulonephritis, result from a cooperative interaction between PMNs and platelets (PLTs). In consequence, we hypothesized that fibrinogen (Fg) might play a critical role in this process and, accordingly, we found that defibrination of animals decreased both the acute phase proteinuria in NTN (approximately 70%) as well as the influx of PLTs and PMNs into the glomerulus (approximately 40-50%). In contrast, blockade of the PLT Fg receptor, alpha IIb beta 3, with the RGD peptidomimetic SC-49992 decreased proteinuria (approximately 90%) without substantially altering the influx of PMNs or PLTs. Immunocytochemistry showed a marked increase in beta 3 integrin expression in inflamed glomeruli which was prevented either by PMN or PLT depletion before disease induction. FACS and immunocytochemical analysis of glomerular cell dissociates demonstrated that beta 3 integrin expression was predominantly on intraglomerular PLTs. In vitro, activated PLTs stimulated the PMN respiratory burst, an interaction which could be inhibited by Fg receptor blockade. In sum, acute NTN is accompanied by a marked increase in glomerular beta 3 integrin expression predominantly due to the influx of PLTs which localize to the glomerulus in a PMN-dependent fashion. Fg appears to serve a major role as a coactivating stimulus for PLT-PMNs in situ via alpha IIb beta 3, potentially mediating the PMN respiratory burst which contributes to proteinuria. Fg may also play a subsidiary role in PMN/PLT comigration.

Indexed as

AnimalsAntigen-Antibody ComplexBlood PlateletsComplement C3DipeptidesFibrinogenGlomerulonephritisImmunoglobulin GIntegrin beta3IntegrinsKidney GlomerulusLeukocyte Common AntigensNeutrophilsOligopeptidesPlatelet AdhesivenessPlatelet Aggregation Inhibitors8-guanidino-octanoyl-Asp-PheAntigen-Antibody Complexarginyl-glycyl-aspartyl-phenylalanineComplement C3DipeptidesFibrinogenImmunoglobulin GIntegrin beta3IntegrinsLeukocyte Common AntigensOligopeptidesPlatelet Aggregation Inhibitors

Identifiers

PMID8083378
PMCPMC295129
OpenAlexW2154499693

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.