Evidence map›Paper›PMID 31356784›Full record

ReviewBrain research2019

Effects of angiotensin-II on brain endothelial cell permeability via PPARalpha regulation of para- and trans-cellular pathways.

Shuzhen Guo, Angel T Som, Ken Arai, Eng H Lo

Open access · greenAbstract readReview
In one paragraph

Review in Brain research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  5. Angiotensin III induces disruption of blood-brain barrier integrity in vitro in bEnd.3 brain endothelial cells.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
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  9. Alterations of the blood-brain barrier during aging.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Review
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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

4 authors at 1 institution in 1 country.

Shuzhen GuoNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, United States. Electronic address: sguo@mgh.harvard.edu.
Angel T SomNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, United States.
Ken AraiNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, United States.
Eng H LoNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, United States. Electronic address: Lo@helix.mgh.harvard.edu.
Harvard University · US

Funding

Targeting ROCK for Neurogliovascular Plasticity & Remodeling After StrokeP01NS055104 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H. · 2007 to 2018
$13.3M
Proteomic Profiling of Patent Foramen Ovale Related Neurovascular InjuryR01NS067139 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI NING, MINGMING · 2010 to 2023
$3.7M
Thrombolysis Profiles in tPA ResponseR01NS093415 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H., NING, MINGMING · 2015 to 2019
$1.9M
Glycoproteomics in Ischemic Stroke Related HyperglycemiaR21NS113065 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI NING, MINGMING · 2020 to 2020
$462k
NINDS NIH HHS P01 NS055104NINDS NIH HHS R01 NS067139NINDS NIH HHS R01 NS093415NINDS NIH HHS R21 NS113065
6 · The paper itself

Abstract

Angiotensin-II (Ang-II) is a key factor in hypertension, diabetes and aging, which are all primary risk factors for CNS disease. Furthermore, Ang-II may play under-appreciated roles in neurogenesis, angiogenesis and CNS remodeling. Therefore, any contemplated attempts for neurorestorative therapies in the CNS should consider the context of Ang-II signaling. Here, we investigate how Ang-II may regulate cerebral endothelial permeability, a key functional feature of the neurovascular unit. Exposure of human brain endothelial cell cultures to Ang-II increased its permeability to BSA-Alexa488 tracer. Immunocytochemistry and pulse-chase experiments suggested that both para-cellular as well as trans-cellular pathways were involved. Candesartan but not PD123319 blocked Ang-II permeability effects, suggesting that Ang-II effects may be mediated via type 1 receptor. Immunocytochemistry and western blots showed that Ang-II disrupted the membrane distributions of ZO-1 and VE-Cad, decreased total levels of JAM-A and Mfsd2a, and increased Cav1. These effects of Ang-II were accompanied by dephosphorylation of PPARalpha. Finally, Ang-II-induced increases in endothelial permeability were ameliorated by PPARalpha agonists. Taken together, these studies suggest that Ang-II may disrupt both para- and trans-cellular permeability in cerebral endothelium, and PPARalpha-related pathways may offer potential therapeutic targets for ameliorating these effects in cell-based regenerative medicine.

Indexed as

Capillary PermeabilityAngiotensin IIBrainCell Membrane PermeabilityCells, CulturedEndothelial CellsHumansPPAR alphaSignal TransductionAngiotensin IIPPAR alphaPPARA protein, humanBlood-brain barrierCell therapyGrowth factorNeurovascular unitStroke recovery

Identifiers

PMID31356784
PMCPMC6755037
OpenAlexW2965662275

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.