Evidence map›Paper›PMID 22815829›Full record

ArticlePloS one2012

An IP-10 (CXCL10)-derived peptide inhibits angiogenesis.

Cecelia C Yates-Binder, Margaret Rodgers, Jesse Jaynes, Alan Wells, Richard J Bodnar, Timothy Turner

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Prognostic and predictive values of CXCL10 in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Pooled it
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  15. Physiological and Pathological Remodeling of Cerebral Microvessels.International journal of molecular sciences · 2022
    Review
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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

6 authors at 4 institutions in 1 country.

Cecelia C Yates-BinderTuskegee University, Center for Cancer Research, Tuskegee, Alabama, United States of America. cey4@pitt.edu
Margaret Rodgers
Jesse Jaynes
Alan Wells
Richard J Bodnar
Timothy Turner
University of Pittsburgh · USVA Pittsburgh Healthcare System · USCenter for Cancer Research · USTuskegee University · US

Funding

Dermal-Epidermal Communication during Wound HealingR01GM063569 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WELLS, ALAN · 2003 to 2018
$3.7M
NIGMS NIH HHS R01 GM063569NIGMS NIH HHS R01GM063569
6 · The paper itself

Abstract

Angiogenesis plays a critical role in processes such as organ development, wound healing, and tumor growth. It requires well-orchestrated integration of soluble and matrix factors and timely recognition of such signals to regulate this process. Previous work has shown that newly forming vessels express the chemokine receptor CXC receptor 3 (CXCR3) and, activation by its ligand IP-10 (CXCL10), both inhibits development of new vasculature and causes regression of newly formed vessels. To identify and develop new therapeutic agents to limit or reverse pathological angiogenesis, we identified a 21 amino acid fragment of IP-10, spanning the α-helical domain residues 77-98, that mimic the actions of the whole IP-10 molecule on endothelial cells. Treatment of the endothelial cells with the 22 amino acid fragment referred to as IP-10p significantly inhibited VEGF-induced endothelial motility and tube formation in vitro, properties critical for angiogenesis. Using a Matrigel plug assay in vivo, we demonstrate that IP-10p both prevented vessel formation and induced involution of nascent vessels. CXCR3 neutralizing antibody was able to block the inhibitory effects of the IP-10p, demonstrating specificity of the peptide. Inhibition of endothelial function by IP-10p was similar to that described for IP-10, secondary to CXCR3-mediated increase in cAMP production, activation of PKA inhibiting cell migration, and inhibition of VEGF-mediated m-calpain activation. IP-10p provides a novel therapeutic agent that inhibits endothelial cell function thus, allowing for the modulation of angiogenesis.

Indexed as

Amino Acid SequenceAngiogenesis InhibitorsAntibodies, NeutralizingCell MovementChemokine CXCL10Cyclic AMPCyclic AMP-Dependent Protein KinasesEndothelial CellsEnzyme ActivationHumansModels, MolecularMolecular Sequence DataNeovascularization, PhysiologicPeptidesProtein BindingReceptors, CXCR3Angiogenesis InhibitorsAntibodies, NeutralizingChemokine CXCL10Cyclic AMPCyclic AMP-Dependent Protein KinasesPeptidesReceptors, CXCR3

Identifiers

PMID22815829
PMCPMC3397949
OpenAlexW2008052120

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.