Functional characterization of novel alpha-helical rod domain desmin (DES) pathogenic variants associated with dilated cardiomyopathy, atrioventricular block and a risk for sudden cardiac death.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 04 2021
Historique:
received: 14 09 2020
revised: 02 12 2020
accepted: 07 12 2020
pubmed: 30 12 2020
medline: 29 5 2021
entrez: 29 12 2020
Statut: ppublish

Résumé

Desmin is the major intermediate filament (IF) protein in human heart and skeletal muscle. So-called 'desminopathies' are disorders due to pathogenic variants in the DES gene and are associated with skeletal myopathies and/or various types of cardiomyopathies. So far, only a limited number of DES pathogenic variants have been identified and functionally characterized. Using a Sanger- and next generation sequencing (NGS) approach in patients with various types of cardiomyopathies, we identified two novel, non-synonymous missense DES variants: p.(Ile402Thr) and p.(Glu410Lys). Mutation carriers developed dilated (DCM) or arrhythmogenic cardiomyopathy (ACM), and cardiac conduction disease, leading to spare out the exercise-induced polymorphic ventricular tachycardia; we moved this variant to data in brief. To investigate the functional impact of these four DES variants, transfection experiments using SW-13 and H9c2 cells with native and mutant desmin were performed and filament assembly was analyzed by confocal microscopy. The DES_p.(Ile402Thr) and DES_p.(Glu410Lys) cells showed filament assembly defects forming cytoplasmic desmin aggregates. Furthermore, immunohistochemical and ultrastructural analysis of myocardial tissue from mutation carriers with the DES_p.(Glu410Lys) pathogenic variant supported the in vitro results. Our in vitro results supported the classification of DES_p.(Ile402Thr) and DES_p.(Glu410Lys) as novel pathogenic variants and demonstrated that the cardiac phenotypes associated with DES variants are diverse and cell culture experiments improve in silico analysis and genetic counseling because the pathogenicity of a variant can be clarified.

Sections du résumé

BACKGROUND
Desmin is the major intermediate filament (IF) protein in human heart and skeletal muscle. So-called 'desminopathies' are disorders due to pathogenic variants in the DES gene and are associated with skeletal myopathies and/or various types of cardiomyopathies. So far, only a limited number of DES pathogenic variants have been identified and functionally characterized.
METHODS AND RESULTS
Using a Sanger- and next generation sequencing (NGS) approach in patients with various types of cardiomyopathies, we identified two novel, non-synonymous missense DES variants: p.(Ile402Thr) and p.(Glu410Lys). Mutation carriers developed dilated (DCM) or arrhythmogenic cardiomyopathy (ACM), and cardiac conduction disease, leading to spare out the exercise-induced polymorphic ventricular tachycardia; we moved this variant to data in brief. To investigate the functional impact of these four DES variants, transfection experiments using SW-13 and H9c2 cells with native and mutant desmin were performed and filament assembly was analyzed by confocal microscopy. The DES_p.(Ile402Thr) and DES_p.(Glu410Lys) cells showed filament assembly defects forming cytoplasmic desmin aggregates. Furthermore, immunohistochemical and ultrastructural analysis of myocardial tissue from mutation carriers with the DES_p.(Glu410Lys) pathogenic variant supported the in vitro results.
CONCLUSIONS
Our in vitro results supported the classification of DES_p.(Ile402Thr) and DES_p.(Glu410Lys) as novel pathogenic variants and demonstrated that the cardiac phenotypes associated with DES variants are diverse and cell culture experiments improve in silico analysis and genetic counseling because the pathogenicity of a variant can be clarified.

Identifiants

pubmed: 33373648
pii: S0167-5273(20)34298-4
doi: 10.1016/j.ijcard.2020.12.050
pii:
doi:

Substances chimiques

Desmin 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

167-174

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no conflict of interest.

Auteurs

Björn Fischer (B)

Institute for Genetics of Heart Disease (IfGH), Department of Cardiovascular Medicine, University Hospital Muenster, Muenster, Germany.

Sven Dittmann (S)

Institute for Genetics of Heart Disease (IfGH), Department of Cardiovascular Medicine, University Hospital Muenster, Muenster, Germany. Electronic address: sven.dittmann@ukmuenster.de.

Andreas Brodehl (A)

Erich and Hanna Klessmann Institute, Heart and Diabetes Center NRW, University Hospital of the Ruhr-University Bochum, Bad Oeynhausen, Germany.

Andreas Unger (A)

Institute of Physiology II, University of Muenster, Germany.

Birgit Stallmeyer (B)

Institute for Genetics of Heart Disease (IfGH), Department of Cardiovascular Medicine, University Hospital Muenster, Muenster, Germany.

Matthias Paul (M)

Department of Cardiology I, University Hospital Muenster, Muenster, Germany.

Guiscard Seebohm (G)

Institute for Genetics of Heart Disease (IfGH), Department of Cardiovascular Medicine, University Hospital Muenster, Muenster, Germany.

Anne Kayser (A)

Institute for Genetics of Heart Disease (IfGH), Department of Cardiovascular Medicine, University Hospital Muenster, Muenster, Germany.

Stefan Peischard (S)

Institute for Genetics of Heart Disease (IfGH), Department of Cardiovascular Medicine, University Hospital Muenster, Muenster, Germany.

Wolfgang A Linke (WA)

Institute of Physiology II, University of Muenster, Germany.

Hendrik Milting (H)

Erich and Hanna Klessmann Institute, Heart and Diabetes Center NRW, University Hospital of the Ruhr-University Bochum, Bad Oeynhausen, Germany.

Eric Schulze-Bahr (E)

Institute for Genetics of Heart Disease (IfGH), Department of Cardiovascular Medicine, University Hospital Muenster, Muenster, Germany.

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