Evidence map›Paper›PMID 24114199›Full record

ArticleAngiogenesis2014

The Semaphorin 4D-Plexin-B1-RhoA signaling axis recruits pericytes and regulates vascular permeability through endothelial production of PDGF-B and ANGPTL4.

Hua Zhou, Ying-Hua Yang, John R Basile

RetractedOpen access · greenAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Angiogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
2.4field-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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Role of Semaphorins in Ischemic Stroke.Frontiers in molecular neuroscience · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Guidance Molecules in Vascular Smooth Muscle.Frontiers in physiology · 2018
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. The role of the semaphorins in cancer.Cell adhesion & migration · 2016
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Hua ZhouDepartment of Oncology and Diagnostic Sciences, University of Maryland Dental School, 650 West Baltimore Street, 7-North, Baltimore, MD, 21201, USA.
Ying-Hua Yang
John R Basile
University of Maryland, Baltimore · USU-M Rogel Cancer Center

Funding

The Role of Semaphorin 4D and Plexin-B1 in Tumor-Induced Angiogenesis.R01CA133162 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI BASILE, JOHN R. · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA133162NCI NIH HHS R01-CA133162
6 · The paper itself

Abstract

Semaphorin 4D (SEMA4D) is a member of a family of transmembrane and secreted proteins that have been shown to act through its receptor Plexin-B1 to regulate axon growth cone guidance, lymphocyte activation, and bone density. SEMA4D is also overexpressed by some malignancies and plays a role in tumor-induced angiogenesis similar to vascular endothelial growth factor (VEGF), a protein that has been targeted as part of some cancer therapies. In an attempt to examine the different effects on tumor growth and vascularity for these two pro-angiogenic factors, we previously noted that while inhibition of both VEGF and SEMA4D restricted tumor vascularity and size, vessels forming under conditions of VEGF blockade retained their association with pericytes while those arising in a background of SEMA4D/Plexin-B1 deficiency did not, an intriguing finding considering that alteration in pericyte association with endothelial cells is an emerging aspect of anti-angiogenic intervention in the treatment of cancer. Here we show through array analysis, immunoblots, migration and co-culture assays and VE-cadherin immunohistochemistry that SEMA4D production by head and neck carcinoma tumor cells induces expression of platelet-derived growth factor-B and angiopoietin-like protein 4 from endothelial cells in a Plexin-B1/Rho-dependent manner, thereby influencing proliferation and differentiation of pericytes and vascular permeability, whereas VEGF lacks these effects. These results partly explain the differences observed between SEMA4D and VEGF in pathological angiogenesis and suggest that targeting SEMA4D function along with VEGF could represent a novel anti-angiogenic therapeutic strategy for the treatment of solid tumors.

Indexed as

Signal TransductionAngiopoietin-Like Protein 4AngiopoietinsAntigens, CDHumansHuman Umbilical Vein Endothelial CellsNeoplasmsNeovascularization, PathologicNerve Tissue ProteinsPericytesProto-Oncogene Proteins c-sisReceptors, Cell SurfacerhoA GTP-Binding ProteinSemaphorinsAngiopoietin-Like Protein 4AngiopoietinsANGPTL4 protein, humanAntigens, CDCD100 antigenNerve Tissue ProteinsPLXNB1 protein, humanProto-Oncogene Proteins c-sisReceptors, Cell SurfacerhoA GTP-Binding ProteinRHOA protein, humanSemaphorins

Identifiers

PMID24114199
PMCPMC3947343
OpenAlexW1981675183

What OpenQuestion holds

Textmetadata
LicenceTDM
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.