Evidence map›Paper›PMID 29203902›Full record

ArticleScientific reports2017

Amniotic fluid stem cell-derived vesicles protect from VEGF-induced endothelial damage.

S Sedrakyan, V Villani, S Da Sacco, N Tripuraneni, S Porta, A Achena, M Lavarreda-Pearce, A Petrosyan, H Soloyan, R E De Filippo and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  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

12 authors at 3 institutions in 2 countries.

S SedrakyanGOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
V VillaniGOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
S Da SaccoGOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
N TripuraneniGOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
S PortaDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy.
A AchenaGOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
M Lavarreda-PearceGOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
A PetrosyanGOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
H SoloyanGOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
R E De FilippoGOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
B BussolatiDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy. benedetta.bussolati@unito.it.
L PerinGOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA. lperin@chla.usc.edu.
Children's Hospital of Los Angeles · USUniversity of Southern California · USUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Injection of amniotic fluid stem cells (AFSC) delays the course of progression of renal fibrosis in animals with Alport Syndrome, enhancing kidney function and improving survival. The mechanisms responsible for these protective outcomes are still largely unknown. Here, we showed that vascular endothelial growth factor (VEGF) signaling within the glomeruli of Alport mice is strongly elevated early on in the disease, causing glomerular endothelial cell damage. Intraventricular injected AFSC that homed within the glomeruli showed strong modulation of the VEGF activity, particularly in glomerular endothelial cells. To investigate this phenomenon we hypothesized that extracellular vesicles (EVs) produced by the AFSC could be responsible for the observed renoprotection. AFSC derived EVs presented exosomal and stem cell markers on their surface membrane, including VEGFR1 and VEGFR2. EVs were able to modulate VEGF in glomerular endothelial cells by effectively trapping the excess VEGF through VEGFR1-binding preventing cellular damage. In contrast, VEGFR1/sVEGFR1 knockout EVs failed to show similar protection, thus indicating that VEGF trapping is a potentially viable mechanism for AFSC-EV mediated renoprotection. Taken together, our findings establish that EVs secreted by AFSC could target a specific signaling pathway within the glomerulus, thus representing a new potential glomerulus-specific targeted intervention.

Indexed as

Extracellular VesiclesAmniotic FluidAnimalsCells, CulturedCoculture TechniquesCreatinineDisease Models, AnimalEndothelial CellsKidney GlomerulusMiceNephritis, HereditaryProteinuriaSignal TransductionStem CellsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1CreatinineVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2

Identifiers

PMID29203902
PMCPMC5715019
OpenAlexW2768856357

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.