Evidence map›Paper›PMID 27357373›Full record

ArticleScientific reports2016

Loss of cortactin causes endothelial barrier dysfunction via disturbed adrenomedullin secretion and actomyosin contractility.

Alexander García Ponce, Alí F Citalán Madrid, Hilda Vargas Robles, Sandra Chánez Paredes, Porfirio Nava, Abigail Betanzos, Alexander Zarbock, Klemens Rottner, Dietmar Vestweber, Michael Schnoor

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 63 citations in OpenAlex.

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  20. Cortactin in Lung Cell Function and Disease.International journal of molecular sciences · 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

10 authors at 4 institutions in 2 countries.

Alexander García PonceDepartment for Molecular Biomedicine, Center of Research and Advanced Studies (CINVESTAV-IPN), 07360 Mexico-City, Mexico.
Alí F Citalán MadridDepartment for Molecular Biomedicine, Center of Research and Advanced Studies (CINVESTAV-IPN), 07360 Mexico-City, Mexico.
Hilda Vargas RoblesDepartment for Molecular Biomedicine, Center of Research and Advanced Studies (CINVESTAV-IPN), 07360 Mexico-City, Mexico.
Sandra Chánez ParedesDepartment for Molecular Biomedicine, Center of Research and Advanced Studies (CINVESTAV-IPN), 07360 Mexico-City, Mexico.
Porfirio NavaDepartment for Physiology, Biophysics and Neurosciences, Center of Research and Advanced Studies (CINVESTAV-IPN), 07360 Mexico-City, Mexico.
Abigail BetanzosDepartment for Infectomics and Molecular Pathogenesis, Center of Research and Advanced Studies (CINVESTAV-IPN), 07360 Mexico-City, Mexico.
Alexander ZarbockDepartment of Anesthesiology, Intensive Care and Pain Medicine, University Clinic of Münster, 48149 Münster, Germany.
Klemens RottnerDivision of Molecular Cell Biology, Zoological Institute, TU Braunschweig, 38106 Braunschweig, Germany.
Dietmar VestweberDepartment for Vascular Cell Biology, Max-Planck-Institute for Molecular Biomedicine, 48149 Münster, Germany.
Michael SchnoorDepartment for Molecular Biomedicine, Center of Research and Advanced Studies (CINVESTAV-IPN), 07360 Mexico-City, Mexico.
Center for Research and Advanced Studies of the National Polytechnic Institute · MXHelmholtz Centre for Infection Research · DEMax Planck Institute for Molecular Biomedicine · DEUniversity Hospital Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Changes in vascular permeability occur during inflammation and the actin cytoskeleton plays a crucial role in regulating endothelial cell contacts and permeability. We demonstrated recently that the actin-binding protein cortactin regulates vascular permeability via Rap1. However, it is unknown if the actin cytoskeleton contributes to increased vascular permeability without cortactin. As we consistently observed more actin fibres in cortactin-depleted endothelial cells, we hypothesised that cortactin depletion results in increased stress fibre contractility and endothelial barrier destabilisation. Analysing the contractile machinery, we found increased ROCK1 protein levels in cortactin-depleted endothelium. Concomitantly, myosin light chain phosphorylation was increased while cofilin, mDia and ERM were unaffected. Secretion of the barrier-stabilising hormone adrenomedullin, which activates Rap1 and counteracts actomyosin contractility, was reduced in plasma from cortactin-deficient mice and in supernatants of cortactin-depleted endothelium. Importantly, adrenomedullin administration and ROCK1 inhibition reduced actomyosin contractility and rescued the effect on permeability provoked by cortactin deficiency in vitro and in vivo. Our data suggest a new role for cortactin in controlling actomyosin contractility with consequences for endothelial barrier integrity.

Indexed as

ActomyosinAdrenomedullinAnimalsCapillary PermeabilityContractile ProteinsCortactinEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsLungMaleMicerap1 GTP-Binding Proteinsrho-Associated KinasesRNA InterferenceRNA, Small InterferingActomyosinADM protein, humanAdrenomedullinContractile ProteinsCortactinCTTN protein, humanCttn protein, mouserap1 GTP-Binding ProteinsRap1 protein, mouserho-Associated KinasesRNA, Small InterferingROCK1 protein, humanShelterin ComplexTelomere-Binding ProteinsTERF2IP protein, human

Identifiers

PMID27357373
PMCPMC4928053
OpenAlexW2470774557

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.