Evidence map›Paper›PMID 27687603›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2016

Endothelial Cells Require CD98 for Efficient Angiogenesis-Brief Report.

Zhongji Liao, Joseph M Cantor

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Possible Role of Extracellular Vesicles in Hepatotoxicity of Acetaminophen.International journal of molecular sciences · 2022
    Article
  7. Article
  8. Reporting Sex and Sex Differences in Preclinical Studies.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  9. Imaging Melphalan Therapy Response in Preclinical Extramedullary Multiple Myeloma withJournal of nuclear medicine : official publication, Society of Nuclear Medicine · 2018
    Article
  10. Article
  11. Vascular Development.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Review
  12. 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

2 authors at 1 institution in 1 country.

Zhongji LiaoFrom the Department of Medicine, University of California San Diego, La Jolla.
Joseph M CantorFrom the Department of Medicine, University of California San Diego, La Jolla. jmcantor@ucsd.edu.
University of California, San Diego · US

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ALAN R. SALTIEL · 2003 to 2026
$40.4M
THROMBUS FORMATION IN BABOONSP01HL031950 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI GRIFFIN, JOHN H · 1985 to 2015
$29.4M
Targeting CD98 in Type 1 DiabetesK01DK090416 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CANTOR, JOSEPH M · 2011 to 2015
$755k
NHLBI NIH HHS P01 HL031950NIDDK NIH HHS K01 DK090416NIDDK NIH HHS P30 DK063491
6 · The paper itself

Abstract

objectiveCD98 regulates integrin signaling and is critical for tumor cell proliferation. It is also expressed on endothelial cells (EC), but its role in angiogenesis is unclear. APPROACH AND

resultsWe used specific genetic targeting and antibody blockade approaches to examine the function of CD98 in EC proliferation, blood vessel growth, and tumor angiogenesis. It is upregulated on angiogenic ECs, and EC-specific deletion of CD98 in mice inhibited tumor growth, retinal angiogenesis, and EC proliferation. Reconstitution with CD98 mutants showed that integrin and CD98 interaction is necessary for EC survival and growth. Moreover, anti-CD98 treatment inhibited vessel formation and reversed EC-assisted tumor growth.

conclusionsOur findings demonstrate a requirement for CD98 in EC growth and suggest that CD98-specific reagents could have a dual anticancer effect: directly by inhibiting tumor cell proliferation and indirectly by preventing tumor angiogenesis.

Indexed as

Neovascularization, PathologicNeovascularization, PhysiologicAngiogenesis InhibitorsAnimalsAntibodiesCarcinoma, Lewis LungCell Line, TumorCell ProliferationFemaleFusion Regulatory Protein 1, Heavy ChainGenotypeHumansHuman Umbilical Vein Endothelial CellsIntegrinsMaleMelanoma, ExperimentalAngiogenesis InhibitorsAntibodiesFusion Regulatory Protein 1, Heavy ChainIntegrinsKDR protein, humanSlc3A2 protein, mouseVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2angiogenesis inhibitorscell proliferationendothelial cellintegrins

Identifiers

PMID27687603
PMCPMC5954993
OpenAlexW2544667864

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.