Evidence map›Paper›PMID 26115013›Full record

ArticlePloS one2015

Characterization of Endothelial Progenitor Cell Interactions with Human Tropoelastin.

Young Yu, Steven G Wise, Praveesuda L Michael, Daniel V Bax, Gloria S C Yuen, Matti A Hiob, Giselle C Yeo, Elysse C Filipe, Louise L Dunn, Kim H Chan and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Small Caliber Compliant Vascular Grafts Based on Elastin-Like Recombinamers forFrontiers in bioengineering and biotechnology · 2019
    Article
  2. Article
  3. Article
  4. Article
  5. Elastomers in vascular tissue engineering.Current opinion in biotechnology · 2016
    Review
  6. 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

14 authors at 4 institutions in 1 country.

Young YuDepartment of Cardiology, Royal Prince Alfred Hospital, Sydney, NSW, 2050, Australia; The Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia.
Steven G WiseThe Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia; School of Molecular Bioscience, University of Sydney, Sydney, NSW, 2006, Australia.
Praveesuda L MichaelThe Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia.
Daniel V BaxSchool of Molecular Bioscience, University of Sydney, Sydney, NSW, 2006, Australia.
Gloria S C YuenThe Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia.
Matti A HiobThe Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia; School of Molecular Bioscience, University of Sydney, Sydney, NSW, 2006, Australia.
Giselle C YeoSchool of Molecular Bioscience, University of Sydney, Sydney, NSW, 2006, Australia.
Elysse C FilipeThe Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia.
Louise L DunnThe Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia.
Kim H ChanDepartment of Cardiology, Royal Prince Alfred Hospital, Sydney, NSW, 2050, Australia; The Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia.
Hamid HajianThe Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia.
David S CelermajerDepartment of Cardiology, Royal Prince Alfred Hospital, Sydney, NSW, 2050, Australia; The Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia.
Anthony S WeissSchool of Molecular Bioscience, University of Sydney, Sydney, NSW, 2006, Australia; Bosch Institute, University of Sydney, Sydney, NSW, 2006, Australia; Charles Perkins Centre, University of Sydney, Sydney, NSW, 2006, Australia.
Martin K C NgDepartment of Cardiology, Royal Prince Alfred Hospital, Sydney, NSW, 2050, Australia; The Heart Research Institute, Sydney, NSW, 2042, Australia; Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia.
University of Sydney · AUThe Heart Research Institute · AURoyal Prince Alfred Hospital · AURobert Bosch (Australia) · AU

Funding

Multifunctional Tropoelastin-Silk Biomaterial SystemsR01EB014283 · NIBIB · TUFTS UNIVERSITY MEDFORD · PI KAPLAN, DAVID L. · 2012 to 2015
$1.2M
NIBIB NIH HHS EB014283NIBIB NIH HHS R01 EB014283
6 · The paper itself

Abstract

The deployment of endovascular implants such as stents in the treatment of cardiovascular disease damages the vascular endothelium, increasing the risk of thrombosis and promoting neointimal hyperplasia. The rapid restoration of a functional endothelium is known to reduce these complications. Circulating endothelial progenitor cells (EPCs) are increasingly recognized as important contributors to device re-endothelialization. Extracellular matrix proteins prominent in the vessel wall may enhance EPC-directed re-endothelialization. We examined attachment, spreading and proliferation on recombinant human tropoelastin (rhTE) and investigated the mechanism and site of interaction. EPCs attached and spread on rhTE in a dose dependent manner, reaching a maximal level of 56±3% and 54±3%, respectively. EPC proliferation on rhTE was comparable to vitronectin, fibronectin and collagen. EDTA, but not heparan sulfate or lactose, reduced EPC attachment by 81±3%, while full attachment was recovered after add-back of manganese, inferring a classical integrin-mediated interaction. Integrin αVβ3 blocking antibodies decreased EPC adhesion and spreading on rhTE by 39±3% and 56±10% respectively, demonstrating a large contribution from this specific integrin. Attachment of EPCs on N-terminal rhTE constructs N25 and N18 accounted for most of this interaction, accompanied by comparable spreading. In contrast, attachment and spreading on N10 was negligible. αVβ3 blocking antibodies reduced EPC spreading on both N25 and N18 by 45±4% and 42±14%, respectively. In conclusion, rhTE supports EPC binding via an integrin mechanism involving αVβ3. N25 and N18, but not N10 constructs of rhTE contribute to EPC binding. The regulation of EPC activity by rhTE may have implications for modulation of the vascular biocompatibility of endovascular implants.

Indexed as

AdultCell AdhesionCell ProliferationCells, CulturedEndothelial Progenitor CellsEndothelium, VascularHumansMaleRecombinant ProteinsStentsTissue ScaffoldsTropoelastinYoung AdultRecombinant ProteinsTropoelastin

Identifiers

PMID26115013
PMCPMC4482626
OpenAlexW758755646

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.