Murine Cardiac Pacemaker Cells
Murine Cardiac Pacemaker Cells - Related Videos
08:52
Generation of Murine Cardiac Pacemaker Cell Aggregates Based on ES-Cell-Programming in Combination with Myh6-Promoter-Selection
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Cited by 13 •
2015
This protocol describes how to produce functional sinus nodal tissue from murine pluripotent stem cells (PSC). T-Box3 (TBX3) overexpression plus cardiac Myosin-heavy-chain (Myh6) promoter antibiotic selection leads to highly pure pacemaker cell aggregates. These “Induced-sinoatrial-bodies” (“iSABs”) contain over 80% pacemaker cells, show highly increased beating rates and are able to pace myocardium ex vivo.
07:26
Isolation of Functional Cardiac Immune Cells
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Cited by 9 •
2011
This method for isolating functional immune cells from the heart provides an alternative to the conventional methods of collagenase digestion, which causes unwanted immune cell activation, resulting in a decreased responsiveness of these cells. Our method of isolation yields functional cardiac immune cells by avoiding problems associated with enzymatic digestion.
13:03
Epigenetic Regulation of Cardiac Differentiation of Embryonic Stem Cells and Tissues
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Cited by 3 •
2016
A fine tuning regulation of gene transcription underlies embryonic cell fate decision. Herein, we describe chromatin immunoprecipitation assays used to investigate epigenetic regulation of both cardiac differentiation of stem cells and cardiac development of mouse embryos.
11:51
Construction of Defined Human Engineered Cardiac Tissues to Study Mechanisms of Cardiac Cell Therapy
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Cited by 16 •
2016
This manuscript describes the creation of defined engineered cardiac tissues using surface marker expression and cell sorting. The defined tissues can then be used in a multi-tissue bioreactor to investigate mechanisms of cardiac cell therapy in order to provide a functional, yet controlled, model system of the human heart.
09:20
Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
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Cited by 2 •
2021
This protocol aims to describe a new methodology to measure intrinsic cardiac firing rate using microelectrode array recording of the whole sinoatrial node tissue to identify pacemaking defects in mice. Pharmacological agents can also be introduced in this method to study their effects on intrinsic pacemaking.
FAQs
Automaticity begins with gradual spontaneous depolarization during diastole. Hyperpolarization-activated cyclic nucleotide-gated, or HCN, channels contribute to this voltage change, while cyclic nucleotide signaling helps regulate their activity. As the membrane potential rises, calcium entry and voltage-gated ion channels activate in a coordinated sequence, allowing pacemaker cells to sustain rhythmic firing rather than simply respond to an external beat.
Calcium entry helps connect the gradual diastolic depolarization to the electrical events that produce each heartbeat cycle. Its timing must work with voltage-gated ion channels so the cell progresses through spontaneous activation in an organized way. Studying this coordination helps explain how altered channel activity could affect firing behavior and cardiac rhythm in murine models.
Autonomic signals adjust the rate at which pacemaker cells complete their spontaneous electrical cycles. They act on an intrinsic rhythm that already arises from HCN-channel activity, calcium entry, and voltage-gated ion-channel activation. This distinction allows researchers to examine both baseline automaticity and externally regulated changes in firing rate when analyzing cardiac rhythm.
Developmental studies can trace how pacemaker lineage specification occurs and then examine how the cells acquire mature electrical properties. This links cellular identity with functional maturation rather than treating pacemaker activity as a fixed trait. The resulting analyses help clarify how developmental changes shape cardiac conduction and how disruptions may contribute to abnormal rhythm.
Researchers can investigate how genetic or environmental changes influence pacemaker-cell development, electrical maturation, and cardiac conduction. A developmental comparison can relate altered conditions to changes in lineage specification or firing-related properties. Murine cells therefore provide a framework for connecting developmental perturbations with outcomes relevant to rhythm regulation, including mechanisms associated with congenital arrhythmias.
Their developmental and electrical properties make these cells useful for exploring regenerative strategies and biological alternatives to electronic pacemakers. Studies can ask how pacemaker lineage and mature function might be supported or recreated after disruption. Findings also provide context for congenital arrhythmia research by linking developmental mechanisms to potential approaches for restoring cardiac rhythm.