Evidence map›Paper›PMID 29566045›Full record

ArticlePloS one2018

TGF-β1/CD105 signaling controls vascular network formation within growth factor sequestering hyaluronic acid hydrogels.

Shane Browne, Amit K Jha, Kurosh Ameri, Sivan G Marcus, Yerem Yeghiazarians, Kevin E Healy

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

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  11. Endothelial Dysfunction in the Context of Blood-Brain Barrier Modeling.Journal of evolutionary biochemistry and physiology · 2022
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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 3 institutions in 2 countries.

Shane BrowneDepartments of Bioengineering and Materials Science and Engineering, University of California, Berkeley, CA, United States of America.
Amit K JhaDepartments of Bioengineering and Materials Science and Engineering, University of California, Berkeley, CA, United States of America.
Kurosh AmeriDepartment of Medicine, University of California, San Francisco, CA, United States of America.
Sivan G MarcusDepartments of Bioengineering and Materials Science and Engineering, University of California, Berkeley, CA, United States of America.
Yerem YeghiazariansDepartment of Medicine, University of California, San Francisco, CA, United States of America.
Kevin E HealyDepartments of Bioengineering and Materials Science and Engineering, University of California, Berkeley, CA, United States of America.ORCID 0000-0002-8524-3671
University of California, Berkeley · USUniversity of California, San Francisco · USOllscoil na Gaillimhe – University of Galway · IE

Funding

Enabling Technologies for hES Cell Self-RenewalR01HL096525 · NHLBI · UNIVERSITY OF CALIFORNIA BERKELEY · PI HEALY, KEVIN EDWARD · 2009 to 2013
$1.8M
NHLBI NIH HHS R01 HL096525NIH HHS R01HL096525
6 · The paper itself

Abstract

Cell-based strategies for the treatment of ischemic diseases are at the forefront of tissue engineering and regenerative medicine. Cell therapies purportedly can play a key role in the neovascularization of ischemic tissue; however, low survival and poor cell engraftment with the host vasculature following implantation limits their potential to treat ischemic diseases. To overcome these limitations, we previously developed a growth factor sequestering hyaluronic acid (HyA)-based hydrogel that enhanced transplanted mouse cardiosphere-derived cell survival and formation of vasculature that anastomosed with host vessels. In this work, we examined the mechanism by which HyA hydrogels presenting transforming growth factor beta-1 (TGF-β1) promoted proliferation of more clinically relevant human cardiosphere-derived cells (hCDC), and their formation of vascular-like networks in vitro. We observed hCDC proliferation and enhanced formation of vascular-like networks occurred in the presence of TGF-β1. Furthermore, production of nitric oxide (NO), VEGF, and a host of angiogenic factors were increased in the presence of TGF-β1. This response was dependent on the co-activity of CD105 (Endoglin) with the TGF-βR2 receptor, demonstrating its role in the process of angiogenic differentiation and vascular organization of hCDC. These results demonstrated that hCDC form vascular-like networks in vitro, and that the induction of vascular networks by hCDC within growth factor sequestering HyA hydrogels was mediated by TGF-β1/CD105 signaling.

Indexed as

Endothelial CellsHydrogelsNeovascularization, PhysiologicCell- and Tissue-Based TherapyCell DifferentiationCell ProliferationCells, CulturedCell SurvivalDrug CompoundingEndoglinHumansHyaluronic AcidMyocardiumMyocytes, CardiacSignal TransductionSpheroids, CellularEndoglinHyaluronic AcidHydrogelsTransforming Growth Factor beta1

Identifiers

PMID29566045
PMCPMC5864059
OpenAlexW2791229556

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.