Evidence map›Paper›PMID 23640575›Full record

ArticleAngiogenesis2013

Inhibition of apelin expression switches endothelial cells from proliferative to mature state in pathological retinal angiogenesis.

Atsushi Kasai, Yuki Ishimaru, Kosuke Higashino, Kohei Kobayashi, Akiko Yamamuro, Yasuhiro Yoshioka, Sadaaki Maeda

Open access · hybridAbstract read
In one paragraph

Article in Angiogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.8field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. The Protective Role of Apelin in the Early Stages of Diabetic Retinopathy.International journal of molecular sciences · 2022
    Article
  7. Article
  8. Review
  9. Review
  10. The Role of Apelin/APJ in a Mouse Model of Oxygen-induced Retinopathy.Investigative ophthalmology & visual science · 2020
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Comparative systems pharmacology of HIF stabilization in the prevention of retinopathy of prematurity.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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 2 institutions in 1 country.

Atsushi KasaiInterdisciplinary Program for Biomedical Sciences, Institute for Academic Initiatives, Osaka University, 1-6 Yamadaoka, Suita, Osaka 565-0871, Japan. kasai@phs.osaka-u.ac.jp
Yuki Ishimaru
Kosuke Higashino
Kohei Kobayashi
Akiko Yamamuro
Yasuhiro Yoshioka
Sadaaki Maeda
Setsunan University · JPOsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recruitment of mural cells such as pericytes to patent vessels with an endothelial lumen is a key factor for the maturation of blood vessels and the prevention of hemorrhage in pathological angiogenesis. To date, our understanding of the specific trigger underlying the transition from cell growth to the maturation phase remains incomplete. Since rapid endothelial cell growth causes pericyte loss, we hypothesized that suppression of endothelial growth factors would both promote pericyte recruitment, in addition to inhibiting pathological angiogenesis. Here, we demonstrate that targeted knockdown of apelin in endothelial cells using siRNA induced the expression of monocyte chemoattractant protein-1 (MCP-1) through activation of Smad3, via suppression of the PI3K/Akt pathway. The conditioned medium of endothelial cells treated with apelin siRNA enhanced the migration of vascular smooth muscle cells, through MCP-1 and its receptor pathway. Moreover, in vivo delivery of siRNA targeting apelin, which causes exuberant endothelial cell proliferation and pathological angiogenesis through its receptor APJ, led to increased pericyte coverage and suppressed pathological angiogenesis in an oxygen-induced retinopathy model. These data demonstrate that apelin is not only a potent endothelial growth factor, but also restricts pericyte recruitment, establishing a new connection between endothelial cell proliferation signaling and a trigger of mural recruitment.

Indexed as

AdipokinesAnalysis of VarianceAnimalsApelinApelin ReceptorsBlotting, WesternChemokine CCL2Culture Media, ConditionedEndothelial CellsGene Knockdown TechniquesImmunohistochemistryIntercellular Signaling Peptides and ProteinsMiceMuscle, Smooth, VascularNeovascularization, PathologicReal-Time Polymerase Chain ReactionAdipokinesApelinApelin ReceptorsApln protein, mouseAplnr protein, mouseChemokine CCL2Culture Media, ConditionedIntercellular Signaling Peptides and ProteinsReceptors, G-Protein-CoupledRNA, Small InterferingSmad3 ProteinSmad3 protein, mouse

Identifiers

PMID23640575
PMCPMC3682100
OpenAlexW1975570024

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.