Evidence map›Paper›PMID 18772335›Full record

ArticleThe American journal of pathology2008

Vascular endothelial growth factor-C, a potential paracrine regulator of glomerular permeability, increases glomerular endothelial cell monolayer integrity and intracellular calcium.

Rebecca R Foster, Sadie C Slater, Jaqualine Seckley, Dontscho Kerjaschki, David O Bates, Peter W Mathieson, Simon C Satchell

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
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  8. Formation of the glomerular microvasculature is regulated by VEGFR-3.American journal of physiology. Renal physiology · 2023
    Article
  9. Article
  10. The lymphatics in kidney health and disease.Nature reviews. Nephrology · 2021
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Vascular Growth Factors and Glomerular Disease.Annual review of physiology · 2016
    Review
  16. Review
  17. 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

7 authors at 4 institutions in 2 countries.

Rebecca R FosterAcademic Renal Unit, Southmead Hospital, Bristol, UK.
Sadie C Slater
Jaqualine Seckley
Dontscho Kerjaschki
David O Bates
Peter W Mathieson
Simon C Satchell
University of Bristol · GBSouthmead Hospital · GBBristol Laboratories (United Kingdom) · GBMedical University of Vienna · AT

Funding

Medical Research Council G0500053Wellcome TrustWellcome Trust 075731
6 · The paper itself

Abstract

We have previously reported expression of vascular endothelial growth factor (VEGF)-A and -C in glomerular podocytes and actions of VEGF-A on glomerular endothelial cells (GEnC) that express VEGF receptor-2 (VEGFR-2). Here we define VEGFR-3 expression in GEnC and investigate the effects of the ligand VEGF-C. Renal cortex and cultured GEnC were examined by microscopy, and both cell and glomerular lysates were assessed by Western blotting. VEGF-C effects on trans-endothelial electrical resistance and albumin flux across GEnC monolayers were measured. The effects of VEGF-C156S, a VEGFR-3-specific agonist, and VEGF-A were also studied. VEGF-C effects on intracellular calcium ([Ca2+]i) were measured using a fluorescence technique, receptor phosphorylation was examined by immunoprecipitation assays, and phosphorylation of myosin light chain-2 and VE-cadherin was assessed by blotting with phospho-specific antibodies. GEnC expressed VEGFR-3 in tissue sections and culture, and VEGF-C increased trans-endothelial electrical resistance in a dose-dependent manner with a maximal effect at 120 minutes of 6.8 Omega whereas VEGF-C156S had no effect. VEGF-C reduced labeled albumin flux by 32.8%. VEGF-C and VEGF-A increased [Ca2+]i by 15% and 39%, respectively. VEGF-C phosphorylated VEGFR-2 but not VEGFR-3, myosin light chain-2, or VE-cadherin. VEGF-C increased GEnC monolayer integrity and increased [Ca2+]i, which may be related to VEGF-C-S particular receptor binding and phosphorylation induction characteristics. These observations suggest that podocytes direct GEnC behavior through both VEGF-C and VEGF-A.

Indexed as

Antigens, CDCadherin 5CadherinsCalciumCalcium SignalingCardiac MyosinsCell LineElectric ImpedanceEndothelial CellsFluorescein-5-isothiocyanateHumansIntracellular SpaceKidney GlomerulusMutant ProteinsMyosin Light ChainsParacrine CommunicationAntigens, CDCadherin 5CadherinsCalciumCardiac MyosinsFluorescein-5-isothiocyanateMutant Proteinsmyosin light chain 2Myosin Light ChainsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor CVascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth Factor Receptor-3

Identifiers

PMID18772335
PMCPMC2543063
OpenAlexW2006818280

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.