Evidence map›Paper›PMID 21270094›Full record

ArticleAmerican journal of physiology. Renal physiology2011

Vitronectin accumulates in the interstitium but minimally impacts fibrogenesis in experimental chronic kidney disease.

Jesús M López-Guisa, Allen C Rassa, Xiaohe Cai, Sarah J Collins, Allison A Eddy

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  10. Inhibition ofJournal of the American Society of Nephrology : JASN · 2017
    Article
  11. Vitronectin-binding PAI-1 protects against the development of cardiac fibrosis through interaction with fibroblasts.Laboratory investigation; a journal of technical methods and pathology · 2014
    Article
  12. Article
  13. Investigating mechanisms of chronic kidney disease in mouse models.Pediatric nephrology (Berlin, Germany) · 2012
    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

5 authors at 2 institutions in 1 country.

Jesús M López-GuisaSeattle Children’s Research Institute, Department of Pediatrics, University of Washington, USA.
Allen C Rassa
Xiaohe Cai
Sarah J Collins
Allison A Eddy
Seattle Children's Hospital · USUniversity of Washington · US

Funding

ROLE OF SCAVENGER RECEPTORS IN RENAL FIBROSISP50DK044757 · NIDDK · VANDERBILT UNIVERSITY · PI FOGO, AGNES B. · 1992 to 2011
$11.5M
NIDDK NIH HHS DK44757NIDDK NIH HHS DK54500NIDDK NIH HHS P50 DK044757
6 · The paper itself

Abstract

Vitronectin (Vtn) is a glycoprotein found in normal serum and pathological extracellular matrix. Given its known interactions with plasminogen activator inhibitor-1 (PAI-1) and Vtn cellular receptors, especially αvβ3 integrin and the urokinase receptor (uPAR), this study was designed to investigate its role in renal fibrogenesis in the mouse model of unilateral ureteral obstruction (UUO). Kidney Vtn mRNA levels were increased ×1.8-5.1 and Vtn protein levels ×1.9-3 on days 7, 14, and 21 after UUO compared with sham kidney levels. Groups of age-matched C57BL/6 wild-type (Vtn+/+) and Vtn-/- mice (n = 10-11/group) were killed 7, 14, or 21 days after UUO. Absence of Vtn resulted in the following significant differences, but only on day 14: fewer αSMA+ interstitial myofibroblasts (×0.53), lower procollagen III mRNA levels (×0.41), lower PAI-1 protein (×0.23), higher uPA activity (×1.1), and lower αv protein (×0.32). The number of CD68+ macrophages did not differ between the genotypes. Despite these transient differences on day 14, the absence of Vtn had no effect on fibrosis severity based on both picrosirius red-positive interstitial area and total kidney collagen measured by the hydroxyproline assay. These findings suggest that despite significant interstitial Vtn deposition in the UUO model of chronic kidney disease, its fibrogenic role is either nonessential or redundant. These data are remarkable given Vtn's strong affinity for the potent fibrogenic molecule PAI-1.

Indexed as

AnimalsChronic DiseaseDisease Models, AnimalFibrosisGenotypeIntegrin alphaVbeta3KidneyKidney DiseasesMacrophagesMiceMice, Inbred C57BLMice, KnockoutMyofibroblastsPhenotypePlasminogen Activator Inhibitor 1Plasminogen ActivatorsIntegrin alphaVbeta3Plasminogen Activator Inhibitor 1Plasminogen ActivatorsReceptors, Urokinase Plasminogen ActivatorRNA, MessengerVimentin

Identifiers

PMID21270094
PMCPMC3094052
OpenAlexW2124090458

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.