Evidence map›Paper›PMID 30044710›Full record

ArticleMolecular biology of the cell2018

Transition of responsive mechanosensitive elements from focal adhesions to adherens junctions on epithelial differentiation.

Barbara Noethel, Lena Ramms, Georg Dreissen, Marco Hoffmann, Ronald Springer, Matthias Rübsam, Wolfgang H Ziegler, Carien M Niessen, Rudolf Merkel, Bernd Hoffmann

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 37 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

10 authors at 3 institutions in 1 country.

Barbara NoethelForschungszentrum Jülich, Institute of Complex Systems, ICS-7: Biomechanics, 52428 Jülich, Germany.
Lena RammsForschungszentrum Jülich, Institute of Complex Systems, ICS-7: Biomechanics, 52428 Jülich, Germany.
Georg DreissenForschungszentrum Jülich, Institute of Complex Systems, ICS-7: Biomechanics, 52428 Jülich, Germany.
Marco HoffmannForschungszentrum Jülich, Institute of Complex Systems, ICS-7: Biomechanics, 52428 Jülich, Germany.
Ronald SpringerForschungszentrum Jülich, Institute of Complex Systems, ICS-7: Biomechanics, 52428 Jülich, Germany.
Matthias RübsamDepartment of Dermatology, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Center for Molecular Medicine Cologne, University of Cologne, 50931 Cologne, Germany.
Wolfgang H ZieglerDepartment of Pediatric Kidney, Liver and Metabolic Diseases, Hannover Medical School, 30625 Hannover, Germany.
Carien M NiessenDepartment of Dermatology, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Center for Molecular Medicine Cologne, University of Cologne, 50931 Cologne, Germany.
Rudolf MerkelForschungszentrum Jülich, Institute of Complex Systems, ICS-7: Biomechanics, 52428 Jülich, Germany.
Bernd HoffmannForschungszentrum Jülich, Institute of Complex Systems, ICS-7: Biomechanics, 52428 Jülich, Germany.
Forschungszentrum Jülich · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The skin's epidermis is a multilayered epithelial tissue and the first line of defense against mechanical stress. Its barrier function depends on an integrated assembly and reorganization of cell-matrix and cell-cell junctions in the basal layer and on different intercellular junctions in suprabasal layers. However, how mechanical stress is recognized and which adhesive and cytoskeletal components are involved are poorly understood. Here, we subjected keratinocytes to cyclic stress in the presence or absence of intercellular junctions. Both states not only recognized but also responded to strain by reorienting actin filaments perpendicular to the applied force. Using different keratinocyte mutant strains that altered the mechanical link of the actin cytoskeleton to either cell-matrix or cell-cell junctions, we show that not only focal adhesions but also adherens junctions function as mechanosensitive elements in response to cyclic strain. Loss of paxillin or talin impaired focal adhesion formation and only affected mechanosensitivity in the absence but not presence of intercellular junctions. Further analysis revealed the adherens junction protein α-catenin as a main mechanosensor, with greatest sensitivity conferred on binding to vinculin. Our data reveal a mechanosensitive transition from cell-matrix to cell-cell adhesions on formation of keratinocyte monolayers with vinculin and α-catenin as vital players.

Indexed as

Cell DifferentiationActinsAdherens Junctionsalpha CateninAnimalsCell CommunicationEpithelial CellsFocal AdhesionsMechanotransduction, CellularMicePaxillinProtein BindingStress FibersStress, MechanicalVinculinActinsalpha CateninPaxillinVinculin

Identifiers

PMID30044710
PMCPMC6249805
OpenAlexW2883495592

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.