Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation.
Sci Transl Med
; 11(493)2019 05 22.
Article
en En
| MEDLINE
| ID: mdl-31118294
ABSTRACT
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.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Fibrilación Atrial
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Cateterismo Cardíaco
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Neuroglía
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Subunidad beta de la Proteína de Unión al Calcio S100
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Miocardio
Límite:
Animals
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Humans
Idioma:
En
Revista:
Sci Transl Med
Asunto de la revista:
CIENCIA
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MEDICINA
Año:
2019
Tipo del documento:
Article
País de afiliación:
Alemania
Pais de publicación:
EEUU
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ESTADOS UNIDOS
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ESTADOS UNIDOS DA AMERICA
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EUA
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UNITED STATES
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UNITED STATES OF AMERICA
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US
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USA