Evidence map›Paper›PMID 26323789›Full record

ArticleScientific reports2015

The Cardiomyopathy Lamin A/C D192G Mutation Disrupts Whole-Cell Biomechanics in Cardiomyocytes as Measured by Atomic Force Microscopy Loading-Unloading Curve Analysis.

Thomas Lanzicher, Valentina Martinelli, Luca Puzzi, Giorgia Del Favero, Barbara Codan, Carlin S Long, Luisa Mestroni, Matthew R G Taylor, Orfeo Sbaizero

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  9. Review
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  11. Atomic Force Microscopy (AFM) Applications in Arrhythmogenic Cardiomyopathy.International journal of molecular sciences · 2022
    Review
  12. Transcriptional Regulation of Cardiac Development and Disease.International journal of molecular sciences · 2022
    Article
  13. Review
  14. Article
  15. Article
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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

9 authors at 4 institutions in 3 countries.

Thomas LanzicherDepartment of Engineering and Architecture, University of Trieste, Via Valerio 2, 34127, Trieste Italy.
Valentina MartinelliInternational Center for Genetic Engineering and Biotechnology, Area di Ricerca, Padriciano 99, 34149 Trieste Italy.
Luca PuzziDepartment of Engineering and Architecture, University of Trieste, Via Valerio 2, 34127, Trieste Italy.
Giorgia Del FaveroDepartment of Food Chemistry and Toxicology, University of Vienna, Waehringer Str. 38 A, 1090 Vienna.
Barbara CodanDepartment of Engineering and Architecture, University of Trieste, Via Valerio 2, 34127, Trieste Italy.
Carlin S LongUniversity of Colorado Cardiovascular Institute, University of Colorado Denver AMC, 12700 East 19th Ave. Aurora 80045, Colorado, USA.
Luisa MestroniUniversity of Colorado Cardiovascular Institute, University of Colorado Denver AMC, 12700 East 19th Ave. Aurora 80045, Colorado, USA.
Matthew R G TaylorUniversity of Colorado Cardiovascular Institute, University of Colorado Denver AMC, 12700 East 19th Ave. Aurora 80045, Colorado, USA.
Orfeo SbaizeroDepartment of Engineering and Architecture, University of Trieste, Via Valerio 2, 34127, Trieste Italy.
University of Trieste · ITUniversity of Colorado Denver · USInternational Centre for Genetic Engineering and Biotechnology · ITUniversity of Vienna · AT

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR025780 · NCRR · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2008 to 2011
$61.3M
Colorado Clinical and Translational Sciences InstituteUL1TR001082 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2013 to 2017
$48.0M
Molecular Epidemiology of Dilated CardiomyopathR01HL069071 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MESTRONI, LUISA · 2002 to 2005
$2.3M
Whole genome DNA sequencing to identify novel genes in dilated cardiomyopathyR01HL109209 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI TAYLOR, MATTHEW R · 2012 to 2016
$2.1M
Cardiomyocyte phenotype and mechanotransduction in Filamin C gene variants causing arrhythmogenic cardiomyopathyR01HL147064 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MESTRONI, LUISA, TAYLOR, MATTHEW R · 2020 to 2023
$2.1M
Familial Dilated Cardiomyopathy:Genetic CharacterizationK23HL067915 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI TAYLOR, MATTHEW R · 2002 to 2006
$653k
NCATS NIH HHS UL1 TR001082NCRR NIH HHS UL1 RR025780NHLBI NIH HHS 1R01HL109209-01A1NHLBI NIH HHS K23 HL067915NHLBI NIH HHS R01 HL069071NHLBI NIH HHS R01 HL109209NHLBI NIH HHS R01 HL147064NHLBI NIH HHS R01 HL69071PHS HHS K23 JL067915
6 · The paper itself

Abstract

Atomic force microscopy (AFM) cell loading/unloading curves were used to provide comprehensive insights into biomechanical behavior of cardiomyocytes carrying the lamin A/C (LMNA) D192G mutation known to cause defective nuclear wall, myopathy and severe cardiomyopathy. Our results suggested that the LMNA D192G mutation increased maximum nuclear deformation load, nuclear stiffness and fragility as compared to controls. Furthermore, there seems to be a connection between this lamin nuclear mutation and cell adhesion behavior since LMNA D192G cardiomyocytes displayed loss of AFM probe-to-cell membrane adhesion. We believe that this loss of adhesion involves the cytoskeletal architecture since our microscopic analyses highlighted that mutant LMNA may also lead to a morphological alteration in the cytoskeleton. Furthermore, chemical disruption of the actin cytoskeleton by cytochalasin D in control cardiomyocytes mirrored the alterations in the mechanical properties seen in mutant cells, suggesting a defect in the connection between the nucleoskeleton, cytoskeleton and cell adhesion molecules in cells expressing the mutant protein. These data add to our understanding of potential mechanisms responsible for this fatal cardiomyopathy, and show that the biomechanical effects of mutant lamin extend beyond nuclear mechanics to include interference of whole-cell biomechanical properties.

Indexed as

AnimalsCardiomyopathiesCell AdhesionCell NucleusCells, CulturedCytochalasin DElastic ModulusHumansLamin Type AMicroscopy, Atomic ForceMutagenesisMyocytes, CardiacRatsCytochalasin DLamin Type A

Identifiers

PMID26323789
PMCPMC4555041
OpenAlexW1266734045

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Registered trials

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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.