Evidence map›Paper›PMID 35476363›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2022

Hypoxia-induced blood-brain barrier dysfunction is prevented by pericyte-conditioned media via attenuated actomyosin contractility and claudin-5 stabilization.

John J Jamieson, YingYu Lin, Nicholas Malloy, Daniel Soto, Peter C Searson, Sharon Gerecht

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 12 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

6 authors at 1 institution in 1 country.

John J JamiesonDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, Maryland, USA.
YingYu LinDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, Maryland, USA.
Nicholas MalloySolomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Daniel SotoSolomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Peter C SearsonInstitute for Nanobiotechnology, Johns Hopkins University, Baltimore, Maryland, USA.ORCID 0000-0002-5417-0828
Sharon GerechtDepartment of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, Maryland, USA.ORCID 0000-0002-8542-4835
Johns Hopkins University · US

Funding

The Role of Physical Cues in Collective Cell InvasionU54CA210173 · NCI · JOHNS HOPKINS UNIVERSITY · PI WIRTZ, DENIS · 2016 to 2020
$9.9M
Mechanisms of cerebrovascular barrier dysfunction caused by APP and PSEN1 mutations and amyloid beta exposureR01NS106008 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SEARSON, PETER C · 2019 to 2023
$1.9M
Reverse engineering zonation-specific and age-specific iPSC-derived cerebrovascular models based on transcriptomic profiling of the human brainR61HL154252 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HEIMAN, MYRIAM, SEARSON, PETER C · 2021 to 2022
$1.6M
NCI NIH HHS U54 CA210173NHLBI NIH HHS R61 HL154252NINDS NIH HHS R01 NS106008
6 · The paper itself

Abstract

The blood-brain barrier (BBB) regulates molecular and cellular entry from the cerebrovasculature into the surrounding brain parenchyma. Many diseases of the brain are associated with dysfunction of the BBB, where hypoxia is a common stressor. However, the contribution of hypoxia to BBB dysfunction is challenging to study due to the complexity of the brain microenvironment. In this study, we used a BBB model with brain microvascular endothelial cells and pericytes differentiated from iPSCs to investigate the effect of hypoxia on barrier function. We found that hypoxia-induced barrier dysfunction is dependent upon increased actomyosin contractility and is associated with increased fibronectin fibrillogenesis. We propose a role for actomyosin contractility in mediating hypoxia-induced barrier dysfunction through modulation of junctional claudin-5. Our findings suggest pericytes may protect brain microvascular endothelial cells from hypoxic stresses and that pericyte-derived factors could be candidates for treatment of pathological barrier-forming tissues.

Indexed as

ActomyosinBlood-Brain BarrierClaudin-5Endothelial CellsPericytesCell HypoxiaCulture Media, ConditionedHumansActomyosinClaudin-5CLDN5 protein, humanCulture Media, Conditionedblood-brain barrierbrain microvascular endothelial cellscontractilityhypoxiainduced pluripotent stem cellspericytestissue engineeringtransendothelial electrical resistance

Identifiers

PMID35476363
PMCPMC9060394
OpenAlexW4224989578

What OpenQuestion holds

Textmetadata
LicenceTDM
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.