STIM1-Ca²⁺ signaling in coronary sinus cardiomyocytes contributes to interatrial conduction.

Zhang, Hengtao

Bryson, Victoria

Luo, Nancy

Sun, Albert Y

Rosenberg, Paul

2024-02-02T17:30:23Z

2024-02-02T17:30:23Z

2020-05

Pacemaker action potentials emerge from the sinoatrial node (SAN) and rapidly propagate through the atria to the AV node via preferential conduction pathways, including one associated with the coronary sinus. However, few distinguishing features of these tracts are known. Identifying specific molecular markers to distinguish among these conduction pathways will have important implications for understanding atrial conduction and atrial arrhythmogenesis. Using a Stim1 reporter mouse, we discovered stromal interaction molecule 1 (STIM1)-expressing coronary sinus cardiomyocytes (CSC)s in a tract from the SAN to the coronary sinus. Our studies here establish that STIM1 is a molecular marker of CSCs and we propose a role for STIM1-CSCs in interatrial conduction. Deletion of Stim1 from the CSCs slowed interatrial conduction and increased susceptibility to atrial arrhythmias. Store-operated Ca²⁺ currents (I_soc) in response to Ca²⁺ store depletion were markedly reduced in CSCs and their action potentials showed electrical remodeling. Our studies identify STIM1 as a molecular marker for a coronary sinus interatrial conduction pathway. We propose a role for SOCE in Ca²⁺ signaling of CSCs and implicate STIM1 in atrial arrhythmogenesis.

S0143-4160(20)30005-1

0143-4160

1532-1991

https://hdl.handle.net/10161/30117

eng

Elsevier BV

Cell calcium

10.1016/j.ceca.2020.102163

https://creativecommons.org/licenses/by-nc/4.0

Heart Atria

Heart Conduction System

Sinoatrial Node

Myocytes, Cardiac

Animals

Mice, Inbred C57BL

Mice, Knockout

Ion Channel Gating

Calcium Signaling

Gene Deletion

Action Potentials

Arrhythmias, Cardiac

Coronary Sinus

Stromal Interaction Molecule 1

STIM1-Ca²⁺ signaling in coronary sinus cardiomyocytes contributes to interatrial conduction.

Journal article

Rosenberg, Paul|0000-0002-5659-160X

102163

Duke

School of Medicine

Clinical Science Departments

Institutes and Centers

Medicine

Pathology

Medicine, Cardiology

Duke Molecular Physiology Institute

Published

87