Evidence map›Paper›PMID 20688932›Full record

ArticleJournal of the American Society of Nephrology : JASN2010

Overexpression of VEGF165b in podocytes reduces glomerular permeability.

Yan Qiu, Joanne Ferguson, Sebastian Oltean, Chris R Neal, Amit Kaura, Heather Bevan, Emma Wood, Leslie M Sage, Silvia Lanati, Dawid G Nowak and 3 more

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. VEGF-AThe Journal of physiology · 2017
    Article
  9. VEGF as a Paracrine Regulator of Conventional Outflow Facility.Investigative ophthalmology & visual science · 2017
    Article
  10. Antiangiogenic Therapy for Diabetic Nephropathy.BioMed research international · 2017
    Review
  11. Vascular Growth Factors and Glomerular Disease.Annual review of physiology · 2016
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Biophysical properties of normal and diseased renal glomeruli.American journal of physiology. Cell physiology · 2011
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 1 institution.

Yan QiuMicrovascular Research Laboratories, Department Physiology and Pharmacology, Bristol Heart Institute, Preclinical Veterinary School, Southwell Street, Bristol, BS2 8EJ, UK.
Joanne Ferguson
Sebastian Oltean
Chris R Neal
Amit Kaura
Heather Bevan
Emma Wood
Leslie M Sage
Silvia Lanati
Dawid G Nowak
Andy H J Salmon
David Bates
Steve J Harper
University of Arizona Cancer Center

Funding

British Heart Foundation BS/06/005British Heart Foundation FS/04/09British Heart Foundation FS/05/114/19959British Heart Foundation FS/07/059/24071British Heart Foundation PG08/022/21636Medical Research Council G0600920Medical Research Council G0802829Medical Research Council GR0600920Wellcome TrustWellcome Trust 69029Wellcome Trust 69134
6 · The paper itself

Abstract

The observation that therapeutic agents targeting vascular endothelial growth factor-A (VEGF-A) associate with renal toxicity suggests that VEGF plays a role in the maintenance of the glomerular filtration barrier. Alternative mRNA splicing produces the VEGF(xxx)b family, which consists of antiangiogenic peptides that reduce permeability and inhibit tumor growth; the contribution of these peptides to normal glomerular function is unknown. Here, we established and characterized heterozygous and homozygous transgenic mice that overexpress VEGF(165)b specifically in podocytes. We confirmed excess production of glomerular VEGF(165)b by reverse transcriptase-PCR, immunohistochemistry, and ELISA in both heterozygous and homozygous animals. Macroscopically, the mice seemed normal up to 18 months of age, unlike the phenotype of transgenic podocyte-specific VEGF(164)-overexpressing mice. Animals overexpressing VEGF(165)b, however, had a significantly reduced normalized glomerular ultrafiltration fraction with accompanying changes in ultrastructure of the glomerular filtration barrier on the vascular side of the glomerular basement membrane. These data highlight the contrasting properties of VEGF splice variants and their impact on glomerular function and phenotype.

Indexed as

Alternative SplicingAnimalsKidney GlomerulusMiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicPermeabilityPodocytesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor A

Identifiers

PMID20688932
PMCPMC3013528
OpenAlexW2139359754

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.