Paclitaxel mitigates structural alterations and cardiac conduction system defects in a mouse model of Hutchinson-Gilford progeria syndrome.


Journal

Cardiovascular research
ISSN: 1755-3245
Titre abrégé: Cardiovasc Res
Pays: England
ID NLM: 0077427

Informations de publication

Date de publication:
29 01 2022
Historique:
received: 01 06 2020
revised: 11 11 2020
accepted: 09 02 2021
pubmed: 25 2 2021
medline: 3 3 2022
entrez: 24 2 2021
Statut: ppublish

Résumé

Hutchinson-Gilford progeria syndrome (HGPS) is an ultrarare laminopathy caused by expression of progerin, a lamin A variant, also present at low levels in non-HGPS individuals. HGPS patients age and die prematurely, predominantly from cardiovascular complications. Progerin-induced cardiac repolarization defects have been described previously, although the underlying mechanisms are unknown. We conducted studies in heart tissue from progerin-expressing LmnaG609G/G609G (G609G) mice, including microscopy, intracellular calcium dynamics, patch-clamping, in vivo magnetic resonance imaging, and electrocardiography. G609G mouse cardiomyocytes showed tubulin-cytoskeleton disorganization, t-tubular system disruption, sarcomere shortening, altered excitation-contraction coupling, and reductions in ventricular thickening and cardiac index. G609G mice exhibited severe bradycardia, and significant alterations of atrio-ventricular conduction and repolarization. Most importantly, 50% of G609G mice had altered heart rate variability, and sinoatrial block, both significant signs of premature cardiac aging. G609G cardiomyocytes had electrophysiological alterations, which resulted in an elevated action potential plateau and early afterdepolarization bursting, reflecting slower sodium current inactivation and long Ca+2 transient duration, which may also help explain the mild QT prolongation in some HGPS patients. Chronic treatment with low-dose paclitaxel ameliorated structural and functional alterations in G609G hearts. Our results demonstrate that tubulin-cytoskeleton disorganization in progerin-expressing cardiomyocytes causes structural, cardiac conduction, and excitation-contraction coupling defects, all of which can be partially corrected by chronic treatment with low dose paclitaxel.

Identifiants

pubmed: 33624748
pii: 6149085
doi: 10.1093/cvr/cvab055
pmc: PMC8803078
doi:

Substances chimiques

Anti-Arrhythmia Agents 0
Lamin Type A 0
Lmna protein, mouse 0
Tubulin 0
Paclitaxel P88XT4IS4D

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

503-516

Subventions

Organisme : NIA NIH HHS
ID : P30 AG024824
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL122352
Pays : United States

Informations de copyright

© The Author(s) 2021. Published by Oxford University Press on behalf of the European Society of Cardiology.

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Auteurs

Álvaro Macías (Á)

Vascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.

J Jaime Díaz-Larrosa (JJ)

Vascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.

Yaazan Blanco (Y)

Vascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.

Víctor Fanjul (V)

Vascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.

Cristina González-Gómez (C)

Vascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.
CIBER en Enfermedades Cardiovasculares (CIBER-CV), Madrid, Spain.

Pilar Gonzalo (P)

Vascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.

María Jesús Andrés-Manzano (MJ)

Vascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.
CIBER en Enfermedades Cardiovasculares (CIBER-CV), Madrid, Spain.

Andre Monteiro da Rocha (AM)

Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI 48109-2800, USA.

Daniela Ponce-Balbuena (D)

Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI 48109-2800, USA.

Andrew Allan (A)

Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI 48109-2800, USA.

David Filgueiras-Rama (D)

CIBER en Enfermedades Cardiovasculares (CIBER-CV), Madrid, Spain.
Department of Cardiology, Cardiac Electrophysiology Unit, Hospital Clínico San Carlos, 28040 Madrid, Spain.
Myocardial, Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.

José Jalife (J)

CIBER en Enfermedades Cardiovasculares (CIBER-CV), Madrid, Spain.
Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI 48109-2800, USA.
Myocardial, Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.

Vicente Andrés (V)

Vascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.
CIBER en Enfermedades Cardiovasculares (CIBER-CV), Madrid, Spain.

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Classifications MeSH