Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation.
Action Potentials
Animals
Atrial Fibrillation
/ blood
Autonomic Nervous System
/ pathology
Cardiac Catheterization
Catheter Ablation
Humans
Mice, Inbred C57BL
Myocardium
/ pathology
Myocytes, Cardiac
/ pathology
Neurites
/ metabolism
Neuroglia
/ metabolism
S100 Calcium Binding Protein beta Subunit
/ blood
Journal
Science translational medicine
ISSN: 1946-6242
Titre abrégé: Sci Transl Med
Pays: United States
ID NLM: 101505086
Informations de publication
Date de publication:
22 05 2019
22 05 2019
Historique:
received:
18
10
2018
accepted:
12
04
2019
entrez:
24
5
2019
pubmed:
24
5
2019
medline:
27
6
2020
Statut:
ppublish
Résumé
Atrial fibrillation (AF), the most common sustained heart rhythm disorder worldwide, is linked to dysfunction of the intrinsic cardiac autonomic nervous system (ICNS). The role of ICNS damage occurring during catheter-based treatment of AF, which is the therapy of choice for many patients, remains controversial. We show here that the neuronal injury marker S100B is expressed in cardiac glia throughout the ICNS and is released specifically upon catheter ablation of AF. Patients with higher S100B release were more likely to be AF free during follow-up. Subsequent in vitro studies revealed that murine intracardiac neurons react to S100B with diminished action potential firing and increased neurite growth. This suggests that release of S100B from cardiac glia upon catheter-based treatment of AF is a hallmark of acute neural damage that contributes to nerve sprouting and can be used to assess ICNS damage.
Identifiants
pubmed: 31118294
pii: 11/493/eaav7770
doi: 10.1126/scitranslmed.aav7770
pii:
doi:
Substances chimiques
S100 Calcium Binding Protein beta Subunit
0
Types de publication
Clinical Trial
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIH HHS
ID : OT2 OD023848
Pays : United States
Informations de copyright
Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.