Evidence map›Paper›PMID 25559145›Full record

ArticleCytotherapy2015

Notch ligand Delta-like 1 promotes in vivo vasculogenesis in human cord blood-derived endothelial colony forming cells.

Hyojin Kim, Lan Huang, Paul J Critser, Zhenyun Yang, Rebecca J Chan, Lin Wang, Nadia Carlesso, Sherry L Voytik-Harbin, Irwin D Bernstein, Mervin C Yoder

Open access · greenAbstract read
In one paragraph

Article in Cytotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-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

13 citing papers in PubMed, 29 citations in OpenAlex.

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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

10 authors at 4 institutions in 1 country.

Hyojin KimDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, USA; Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA; Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA; Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Lan HuangDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, USA; Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA; Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Paul J CritserDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, USA; Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Zhenyun YangDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, USA; Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Rebecca J ChanDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, USA; Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Lin WangDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, USA; Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA; Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Nadia CarlessoDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, USA; Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA; Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Sherry L Voytik-HarbinWeldon School of Biomedical Engineering, Purdue University, West Lafayette, Indiana, USA.
Irwin D BernsteinFred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Mervin C YoderDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana, USA; Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA; Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA. Electronic address: myoder@iu.edu.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · USFred Hutch Cancer Center · USPurdue University West Lafayette · US

Funding

Physiologic Regulation of Hematopoiesis by NotchR01DK097837 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI CARLESSO, NADIA · 2014 to 2017
$1.6M
Collagen Cross-links Direct Matrix-Induced Vasculogenesis Via Tunable PathwaysR01HL109602 · NHLBI · PURDUE UNIVERSITY · PI VOYTIK-HARBIN, SHERRY L, YODER, MERVIN C. · 2011 to 2014
$1.5M
NHLBI NIH HHS R01 HL109602NIDDK NIH HHS R01 DK097837
6 · The paper itself

Abstract

BACKGROUND

aimsHuman cord blood (CB) is enriched in circulating endothelial colony forming cells (ECFCs) that display high proliferative potential and in vivo vessel forming ability. Because Notch signaling is critical for embryonic blood vessel formation in utero, we hypothesized that Notch pathway activation may enhance cultured ECFC vasculogenic properties in vivo.

methodsIn vitro ECFC stimulation with an immobilized chimeric Notch ligand (Delta-like1(ext-IgG)) led to significant increases in the mRNA and protein levels of Notch regulated Hey2 and EphrinB2 that were blocked by treatment with γ-secretase inhibitor addition. However, Notch stimulated preconditioning in vitro failed to enhance ECFC vasculogenesis in vivo. In contrast, in vivo co-implantation of ECFCs with OP9-Delta-like 1 stromal cells that constitutively expressed the Notch ligand delta-like 1 resulted in enhanced Notch activated ECFC-derived increased vessel density and enlarged vessel area in vivo, an effect not induced by OP9 control stromal implantation.

resultsThis Notch activation was associated with diminished apoptosis in the exposed ECFC.

conclusionsWe conclude that Notch pathway activation in ECFC in vivo via co-implanted stromal cells expressing delta-like 1 promotes vasculogenesis and augments blood vessel formation via diminishing apoptosis of the implanted ECFC.

Indexed as

Neovascularization, PhysiologicAnimalsCalcium-Binding ProteinsCells, CulturedCollagenColony-Forming Units AssayEndothelial CellsFetal BloodHumansInfant, NewbornIntercellular Signaling Peptides and ProteinsLigandsMembrane ProteinsMice, Inbred NODMice, SCIDRatsCalcium-Binding ProteinsCollagenDLK1 protein, humanIntercellular Signaling Peptides and ProteinsLigandsMembrane ProteinsReceptors, NotchRNA, Messengerapoptosisendothelial colony forming cells (ECFCs)Notch ligand delta-like 1 (Dll1)OP9-Delta-like 1 stromal cells (OP9-DL1)vasculogenesis

Identifiers

PMID25559145
PMCPMC4915927
OpenAlexW2054128108

What OpenQuestion holds

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Registered trials

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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.