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Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation

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Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation. / Scherschel, Katharina; Hedenus, Katja; Jungen, Christiane; Lemoine, Marc D; Rübsamen, Nicole; Veldkamp, Marieke W; Klatt, Niklas; Lindner, Diana; Westermann, Dirk; Casini, Simona; Kuklik, Pawel; Eickholt, Christian; Klöcker, Nikolaj; Shivkumar, Kalyanam; Christ, Torsten; Zeller, Tanja; Willems, Stephan; Meyer, Christian.

In: SCI TRANSL MED, Vol. 11, No. 493, 22.05.2019.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Scherschel, K, Hedenus, K, Jungen, C, Lemoine, MD, Rübsamen, N, Veldkamp, MW, Klatt, N, Lindner, D, Westermann, D, Casini, S, Kuklik, P, Eickholt, C, Klöcker, N, Shivkumar, K, Christ, T, Zeller, T, Willems, S & Meyer, C 2019, 'Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation', SCI TRANSL MED, vol. 11, no. 493. https://doi.org/10.1126/scitranslmed.aav7770

APA

Scherschel, K., Hedenus, K., Jungen, C., Lemoine, M. D., Rübsamen, N., Veldkamp, M. W., Klatt, N., Lindner, D., Westermann, D., Casini, S., Kuklik, P., Eickholt, C., Klöcker, N., Shivkumar, K., Christ, T., Zeller, T., Willems, S., & Meyer, C. (2019). Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation. SCI TRANSL MED, 11(493). https://doi.org/10.1126/scitranslmed.aav7770

Vancouver

Scherschel K, Hedenus K, Jungen C, Lemoine MD, Rübsamen N, Veldkamp MW et al. Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation. SCI TRANSL MED. 2019 May 22;11(493). https://doi.org/10.1126/scitranslmed.aav7770

Bibtex

@article{1ac69fce3e3842e18f0ae0310888915a,
title = "Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation",
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.",
author = "Katharina Scherschel and Katja Hedenus and Christiane Jungen and Lemoine, {Marc D} and Nicole R{\"u}bsamen and Veldkamp, {Marieke W} and Niklas Klatt and Diana Lindner and Dirk Westermann and Simona Casini and Pawel Kuklik and Christian Eickholt and Nikolaj Kl{\"o}cker and Kalyanam Shivkumar and Torsten Christ and Tanja Zeller and Stephan Willems and Christian Meyer",
note = "Copyright {\textcopyright} 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.",
year = "2019",
month = may,
day = "22",
doi = "10.1126/scitranslmed.aav7770",
language = "English",
volume = "11",
journal = "SCI TRANSL MED",
issn = "1946-6234",
publisher = "AMER ASSOC ADVANCEMENT SCIENCE",
number = "493",

}

RIS

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

N1 - Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.

PY - 2019/5/22

Y1 - 2019/5/22

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.

U2 - 10.1126/scitranslmed.aav7770

DO - 10.1126/scitranslmed.aav7770

M3 - SCORING: Journal article

C2 - 31118294

VL - 11

JO - SCI TRANSL MED

JF - SCI TRANSL MED

SN - 1946-6234

IS - 493

ER -