Evidence map›Paper›PMID 15258770›Full record

ArticleHistochemistry and cell biology2004

Alteration of podocytes in a murine model of crescentic glomerulonephritis.

Valérie Besse-Eschmann, Michel Le Hir, Nicole Endlich, Karlhans Endlich

Abstract read
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In one paragraph

Article in Histochemistry and cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Protective Role of Nrf2 in Renal Disease.Antioxidants (Basel, Switzerland) · 2020
    Review
  2. Urinary podocyte and TGF-β1 mRNA as markers for disease activity and progression in anti-glomerular basement membrane nephritis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017
    Article
  3. Are podocytes motile?Pflugers Archiv : European journal of physiology · 2017
    Review
  4. Article
  5. Article
  6. Sirtuin1 Maintains Actin Cytoskeleton by Deacetylation of Cortactin in Injured Podocytes.Journal of the American Society of Nephrology : JASN · 2015
    Article
  7. Ultrastructural pathological features of unilateral renal artery stenosis in the rats.International journal of clinical and experimental pathology · 2015
    Article
  8. Article
  9. Update on crescentic glomerulonephritis.Seminars in immunopathology · 2014
    Review
  10. Two-photon microscopy reveals stationary podocytes in living zebrafish larvae.Journal of the American Society of Nephrology : JASN · 2014
    Article
  11. Parietal epithelial cell activation marker in early recurrence of FSGS in the transplant.Clinical journal of the American Society of Nephrology : CJASN · 2012
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. News and views in Histochemistry and Cell Biology.Histochemistry and cell biology · 2004
    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

4 authors at 2 institutions in 2 countries.

Valérie Besse-EschmannInstitute of Anatomy, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Michel Le Hir
Nicole Endlich
Karlhans Endlich
Heidelberg University · DEUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent observations suggest a central role of podocytes in crescent formation. In experimental glomerulonephritis podocytes disrupt the parietal epithelial layer and attach on its basement membrane, thus forming bridges between the tuft and Bowman's capsule, and they are a major constituent of crescents. In order to explain these findings we hypothesize that inflammation triggers motility in podocytes. In the present study we asked whether podocytes display alterations which suggest a migratory behavior in glomerulonephritis. Glomerulonephritis was induced in mice by injection of a rabbit serum against the glomerular basement membrane. The kidneys were perfusion-fixed 6 days later and examined by light and electron microscopy as well as by immunohistochemistry. In glomerulonephritis the apical cytoplasm of podocytes displayed numerous actin-containing microprotrusions. Cortactin, a protein involved in the regulation of actin polymerization, was predominantly expressed in foot processes of podocytes in control mice. It was redistributed to the cell body in glomerulonephritis. In untreated mice betal-integrin was restricted to the foot processes. In glomerulonephritis it was additionally found in the cytoplasm and in the apical cell membrane. Recycling of integrins is a crucial event in initiation of cell migration. ICAM-1 and CD44, the ligation of which induces migratory behaviors, were absent from healthy podocytes but expressed by some podocytes in glomerulonephritis. Thus, in glomerulonephritis podocytes display some characteristic features of migrating cells. This might explain their ability to break through the parietal epithelium and to become a constituent of early crescents.

Indexed as

ActinsAnimalsCell MovementCell NucleusCells, CulturedCortactinFemaleFluorescent Antibody TechniqueGlomerulonephritisHyaluronan ReceptorsImmunoglobulin GIntegrin beta1Intercellular Adhesion Molecule-1MiceMice, Inbred C57BLMicrofilament ProteinsActinsCortactinCttn protein, mouseHyaluronan ReceptorsImmunoglobulin GIntegrin beta1Intercellular Adhesion Molecule-1Microfilament Proteins

Identifiers

PMID15258770
OpenAlexW2034433703

What OpenQuestion holds

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Registered trials

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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.