TY - JOUR
T1 - Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation
AU - Scherschel, Katharina
AU - Hedenus, Katja
AU - Jungen, Christiane
AU - Lemoine, Marc D.
AU - Rübsamen, Nicole
AU - Veldkamp, Marieke W.
AU - Klatt, Niklas
AU - Lindner, Diana
AU - Westermann, Dirk
AU - Casini, Simona
AU - Kuklik, Pawel
AU - Eickholt, Christian
AU - Klöcker, Nikolaj
AU - Shivkumar, Kalyanam
AU - Christ, Torsten
AU - Zeller, Tanja
AU - Willems, Stephan
AU - Meyer, Christian
PY - 2019
Y1 - 2019
N2 - 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.
AB - 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.
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85066409873&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/31118294
U2 - https://doi.org/10.1126/scitranslmed.aav7770
DO - https://doi.org/10.1126/scitranslmed.aav7770
M3 - Article
C2 - 31118294
SN - 1946-6242
VL - 11
JO - Science translational medicine
JF - Science translational medicine
IS - 493
M1 - eaav7770
ER -