Evidence map›Paper›PMID 30018153›Full record

ArticleEMBO reports2018

PAR-3 controls endothelial planar polarity and vascular inflammation under laminar flow.

Takao Hikita, Fatemeh Mirzapourshafiyi, Pedro Barbacena, Meghan Riddell, Ayesha Pasha, Mengnan Li, Takuji Kawamura, Ralf P Brandes, Tomonori Hirose, Shigeo Ohno and 4 more

Abstract read
In one paragraph

Article in EMBO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

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  5. Junctional adhesion molecule-C: A multifunctional mediator of cell adhesion.Cellular and molecular life sciences : CMLS · 2025
    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

14 authors.

Takao HikitaLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Fatemeh MirzapourshafiyiLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Pedro BarbacenaInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.
Meghan RiddellLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Ayesha PashaLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Mengnan LiLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Takuji KawamuraLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Ralf P BrandesInstitute for Cardiovascular Physiology, Goethe University, Frankfurt am Main, Germany.
Tomonori HiroseDepartment of Molecular Biology, Graduate School of Medical Science Yokohama City University, Yokohama, Japan.
Shigeo OhnoDepartment of Molecular Biology, Graduate School of Medical Science Yokohama City University, Yokohama, Japan.
Holger GerhardtIntegrative Vascular Biology Laboratory, Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0002-3030-0384
Michiyuki MatsudaDepartment of Pathology and Biology of Diseases, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Claudio A FrancoInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.ORCID 0000-0002-2861-3883
Masanori NakayamaLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany masanori.nakayama@mpi-bn.mpg.de.ORCID 0000-0002-0153-7198

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impaired cell polarity is a hallmark of diseased tissue. In the cardiovascular system, laminar blood flow induces endothelial planar cell polarity, represented by elongated cell shape and asymmetric distribution of intracellular organelles along the axis of blood flow. Disrupted endothelial planar polarity is considered to be pro-inflammatory, suggesting that the establishment of endothelial polarity elicits an anti-inflammatory response. However, a causative relationship between polarity and inflammatory responses has not been firmly established. Here, we find that a cell polarity protein, PAR-3, is an essential gatekeeper of GSK3β activity in response to laminar blood flow. We show that flow-induced spatial distribution of PAR-3/aPKCλ and aPKCλ/GSK3β complexes controls local GSK3β activity and thereby regulates endothelial planar polarity. The spatial information for GSK3β activation is essential for flow-dependent polarity to the flow axis, but is not necessary for flow-induced anti-inflammatory response. Our results shed light on a novel relationship between endothelial polarity and vascular homeostasis highlighting avenues for novel therapeutic strategies.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAortaAtherosclerosisCell Adhesion MoleculesCell Cycle ProteinsCell PolarityCytoskeletal ProteinsEndothelium, VascularGene Knockdown TechniquesHEK293 CellsHomeostasisHumansHuman Umbilical Vein Endothelial CellsInflammationMembrane ProteinsAdaptor Proteins, Signal TransducingCell Adhesion MoleculesCell Cycle ProteinsCytoskeletal ProteinsGSKIP protein, mouseMembrane ProteinsNIN protein, humanNuclear ProteinsPARD3 protein, humanPard3 protein, mousePKC-3 proteinProtein Kinase CRepressor Proteinsatherosclerosiscell polarityendothelial cellflowPAR‐3

Identifiers

PMID30018153
PMCPMC6123654

What OpenQuestion holds

Textmetadata
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.