Evidence map›Paper›PMID 24818558›Full record

ArticleScientific reports2014

Recapitulating physiological and pathological shear stress and oxygen to model vasculature in health and disease.

Hasan Erbil Abaci, Yu-I Shen, Scott Tan, Sharon Gerecht

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  19. Article
  20. Collagen fiber structure guides 3D motility of cytotoxic T lymphocytes.Matrix biology : journal of the International Society for Matrix Biology · 2020
    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

4 authors at 1 institution in 1 country.

Hasan Erbil AbaciDepartment of Chemical and Biomolecular Engineering, Johns Hopkins Physical Science Oncology Center and Institute for NanoBioTechnology, The Johns Hopkins University, 3400 N. Charles St., Baltimore, Maryland 21218, USA.
Yu-I ShenDepartment of Chemical and Biomolecular Engineering, Johns Hopkins Physical Science Oncology Center and Institute for NanoBioTechnology, The Johns Hopkins University, 3400 N. Charles St., Baltimore, Maryland 21218, USA.
Scott TanDepartment of Chemical and Biomolecular Engineering, Johns Hopkins Physical Science Oncology Center and Institute for NanoBioTechnology, The Johns Hopkins University, 3400 N. Charles St., Baltimore, Maryland 21218, USA.
Sharon GerechtDepartment of Chemical and Biomolecular Engineering, Johns Hopkins Physical Science Oncology Center and Institute for NanoBioTechnology, The Johns Hopkins University, 3400 N. Charles St., Baltimore, Maryland 21218, USA.
Johns Hopkins University · US

Funding

TRANS NETWORK PROJECTSU54CA143868 · NCI · JOHNS HOPKINS UNIVERSITY · PI WIRTZ, DENIS · 2009 to 2013
$13.7M
Engineered Stem Cell Microenvironments for controlled VasculogenesisR01HL107938 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI GERECHT, SHARON · 2011 to 2015
$2.1M
Strain Specific Detection of Influenza at the Point-of-CareR01EB009764 · NIBIB · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI SOH, HYONGSOK TOM · 2009 to 2012
$1.5M
NCI NIH HHS U54CA143868NIBIB NIH HHS R01-EB-009764
6 · The paper itself

Abstract

Studying human vascular disease in conventional cell cultures and in animal models does not effectively mimic the complex vascular microenvironment and may not accurately predict vascular responses in humans. We utilized a microfluidic device to recapitulate both shear stress and O2 levels in health and disease, establishing a microfluidic vascular model (μVM). Maintaining human endothelial cells (ECs) in healthy-mimicking conditions resulted in conversion to a physiological phenotype namely cell elongation, reduced proliferation, lowered angiogenic gene expression and formation of actin cortical rim and continuous barrier. We next examined the responses of the healthy μVM to a vasotoxic cancer drug, 5-Fluorouracil (5-FU), in comparison with an in vivo mouse model. We found that 5-FU does not induce apoptosis rather vascular hyperpermeability, which can be alleviated by Resveratrol treatment. This effect was confirmed by in vivo findings identifying a vasoprotecting strategy by the adjunct therapy of 5-FU with Resveratrol. The μVM of ischemic disease demonstrated the transition of ECs from a quiescent to an activated state, with higher proliferation rate, upregulation of angiogenic genes, and impaired barrier integrity. The μVM offers opportunities to study and predict human ECs with physiologically relevant phenotypes in healthy, pathological and drug-treated environments.

Indexed as

Oxygen ConsumptionStress, MechanicalAnimalsAtherosclerosisCapillary PermeabilityEndothelial CellsEndothelium, VascularFluorouracilHumansIschemiaMiceMicrofluidic Analytical TechniquesResveratrolStilbenesVascular DiseasesFluorouracilResveratrolStilbenes

Identifiers

PMID24818558
PMCPMC4018609
OpenAlexW2058811019

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.