Evidence map›Paper›PMID 8546219›Full record

ArticleThe American journal of pathology1996

Interferon-inducible protein-10 is highly expressed in rats with experimental nephrosis.

M Gómez-Chiarri, A Ortiz, S González-Cuadrado, D Serón, S N Emancipator, T A Hamilton, A Barat, J J Plaza, E González, J Egido

Abstract read
In one paragraph

Article in The American journal of pathology, 1996. 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
1.4field-weighted citation impact, top 18% 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, 45 citations in OpenAlex.

  1. Article
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  5. Article
  6. Mitogen-Activated Protein Kinase 14 Promotes AKI.Journal of the American Society of Nephrology : JASN · 2017
    Article
  7. Role of Oxidative Stress in Drug-Induced Kidney Injury.International journal of molecular sciences · 2016
    Review
  8. Article
  9. Article
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  12. Article
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  14. Article
  15. Observational
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

10 authors at 5 institutions in 2 countries.

M Gómez-ChiarriFundación Jiménez Díaz, Madrid, Spain.
A Ortiz
S González-Cuadrado
D Serón
S N Emancipator
T A Hamilton
A Barat
J J Plaza
E González
J Egido
Universidad Autónoma de Madrid · ESCase Comprehensive Cancer CenterCase Western Reserve University · USHospital Universitario Fundación Jiménez Díaz · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferon-inducible protein (IP)-10 is a small glycoprotein member of a family of chemotactic cytokines structurally related to interleukin-8. We have recently described the induction of IP-10 mRNA in mouse mesangial cells stimulated with lipopolysacharide, interferon-gamma, and tumor necrosis factor-alpha. To further evaluate a possible role for this chemokine in renal injury, we have studied IP-10 in an experimental model of nephrosis induced in rats by adriamycin. High levels of glomerular IP-10 mRNA expression and glomerular and tubulointerstitial IP-10 protein were seen on day 21, coinciding with maximal proteinuria, glomerular tumor necrosis factor mRNA expression, and interstitial cellular infiltrates. Maintenance on a low protein diet not only delayed the appearance of proteinuria and interstitial cellular infiltrate but also decreased glomerular IP-10 mRNA expression. Isolated normal glomeruli and cultured glomerular epithelial and mesangial cells from normal rats expressed IP-10 mRNA upon stimulation with 100 U/ml interferon or 1 microgram/ml lipopolysaccharide for 3 hours. IP-10 mRNA expression was also inducible by lipopolysaccharide and cytokines in NRK 49F renal interstitial fibroblasts and, to a lesser extent, in NRK 52E tubular epithelial cells. Furthermore, IP-10 protein was inducible in murine mesangial cells. We conclude that IP-10 is highly inducible in vitro and in vivo in resident glomerular and tubulointerstitial cells. IP-10 may participate in the modulation of renal damage in experimental nephrosis.

Indexed as

Chemokines, CXCAnimalsBase SequenceCells, CulturedChemokine CXCL10CytokinesDoxorubicinFemaleImmunophenotypingKidney GlomerulusKidney TubulesLymphocyte ActivationMiceMolecular Sequence DataNephrosisRatsChemokine CXCL10Chemokines, CXCCytokinesDoxorubicinRNA, Messenger

Identifiers

PMID8546219
PMCPMC1861590
OpenAlexW2162177054

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.