ArticleFrontiers in physiology2015
Store-operated calcium entry and the localization of STIM1 and Orai1 proteins in isolated mouse sinoatrial node cells.
Article in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Electrophysiological Mechanisms and Therapeutic Potential of Calcium Channels in Atrial Fibrillation.Reviews in cardiovascular medicine · 2025Review
- How filopodia respond to calcium in the absence of a calcium-binding structural protein: non-channel functions of TRP.Cell communication and signaling : CCS · 2022Article
- The Orai1 inhibitor BTP2 has multiple effects on Ca2+ handling in skeletal muscle.The Journal of general physiology · 2021Article
- Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021Review
- Selective Neuron Vulnerability in Common and Rare Diseases-Mitochondria in the Focus.Frontiers in molecular biosciences · 2021Review
- Genetic Complexity of Sinoatrial Node Dysfunction.Frontiers in genetics · 2021Review
- Targeting Orai1-Mediated Store-Operated CaFrontiers in cell and developmental biology · 2020Review
- Cardiomyocyte-Specific STIM1 (Stromal Interaction Molecule 1) Depletion in the Adult Heart Promotes the Development of Arrhythmogenic Discordant Alternans.Circulation. Arrhythmia and electrophysiology · 2019Article
- Recent progress regarding kaempferol for the treatment of various diseases.Experimental and therapeutic medicine · 2019Review
- Quantitative proteomics and single-nucleus transcriptomics of the sinus node elucidates the foundation of cardiac pacemaking.Nature communications · 2019Article
- SOCE mediated by STIM and Orai is essential for pacemaker activity in the interstitial cells of Cajal in the gastrointestinal tract.Science signaling · 2018Article
- The Complex Role of Store Operated Calcium Entry Pathways and Related Proteins in the Function of Cardiac, Skeletal and Vascular Smooth Muscle Cells.Frontiers in physiology · 2018Review
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
- Protective effects of kaempferol against cardiac sinus node dysfunction via CaMKII deoxidization.Anatomy & cell biology · 2015Article
- STIM1-Ca2+ signaling modulates automaticity of the mouse sinoatrial node.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The involvement of TRPC3 channels in sinoatrial arrhythmias.Frontiers in physiology · 2015Article
- The importance of Ca(2+)-dependent mechanisms for the initiation of the heartbeat.Frontiers in physiology · 2015Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In many non-excitable and excitable cells, store-operated calcium entry (SOCE) represents an additional pathway for calcium entry upon Ca(2+) store depletion. In a previous study, we demonstrated SOCE activity in intact mouse cardiac pacemaker tissue, specifically from sinoatrial node (SAN) tissue. However, store content as a key determinant of SOCE activity is difficult to measure in intact SAN tissue. Therefore, to investigate the interaction between SOCE and store content and its role in cardiac pacemaking, it is necessary to investigate SOCE activity in single cardiac pacemaker cells. Furthermore, recent studies in other tissues have identified two new proteins involved in SOCE, stromal interacting molecule (STIM), which is an ER Ca(2+) sensor, and the surface membrane channel Orai, a prototypic gene encoding for SOCE. However, whether STIM and Orai are expressed in native pacemaker cells is still unknown. In this current study, we examined SOCE activity in single firing pacemaker cells isolated from mouse sinoatrial node tissue. We found a significant rise in Ca(2+) entry in response to Ca(2+) store depletion. SOCE blockers reduced the amplitude and frequency of spontaneous Ca(2+) transients and reduced Ca(2+) store content. We demonstrated for the first time that STIM and Orai are expressed in pacemaker cells. After store depletion, STIM1 redistributed to the cell periphery and showed increased co-localization with surface membrane located Orai1, indicating a possible involvement of these proteins in SOCE activity in native cardiac pacemaker cells. These results suggest the novel concept that SOCE plays a functional role in regulating intracellular Ca(2+) of cardiac pacemaker cells.
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