Adult Rat Cardiomyocytes
Adult Rat Cardiomyocytes - Related Videos
11:06
Isolation and Cultivation of Adult Rat Cardiomyocytes
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Cited by 37 •
2017
Here, we present a protocol for the isolation and cultivation of adult rat ventricular cardiomyocytes (ARVC). Isolated ARVC can be used for short and long-term cultivation. The isolation and cultivation of ARVC can play a key role in developing new treatment regimens for cardiac diseases.
09:38
Simultaneous Isolation of High Quality Cardiomyocytes, Endothelial Cells, and Fibroblasts from an Adult Rat Heart
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Cited by 8 •
2017
Several protocols have been developed and described for the isolation of different cardiac cell types from a rat heart. Here, an optimized protocol is described that allows the isolation of high-quality major cardiac cell types (cardiomyocytes, endothelial cells, and fibroblasts) from a single preparation, reducing the experimental costs.
08:42
Isolation, Culture and Transduction of Adult Mouse Cardiomyocytes
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Cited by 35 •
2016
This protocol describes a step-by-step method for the reproducible isolation and long-term culture of adult mouse cardiomyocytes with high yield, purity, and viability.
07:05
Isolation and Cryopreservation of Neonatal Rat Cardiomyocytes
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Cited by 49 •
2015
The isolation of neonatal rat cardiomyocytes is a time consuming and unpredictable procedure. This study describes methods for cryopreservation and thawing of neonatal rat cardiomyocytes that allows for more efficient use of cells. The thawed NRCMs can be used for various experiments without the need for performing isolations each time.
08:23
Single Cell Transcriptional Profiling of Adult Mouse Cardiomyocytes
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Cited by 13 •
2011
Single cell expression profiling allows the detailed gene expression analysis of individual cells. We describe methods for the isolation of cardiomyocytes, and preparing the resulting lysates for either whole transcriptome microarray or qPCR of specific targets.
FAQs
Contractile activity depends on coordinated structure and signaling rather than on a single cellular feature. Organized sarcomeres provide the mechanical framework, calcium cycling regulates activation and relaxation, and electrical excitation coordinates the timing of contraction. Examining these linked processes helps researchers determine whether an inflammatory or environmental stimulus disrupts cardiac function at the structural, signaling, or excitation level.
Calcium cycling connects cellular excitation with contraction, making it a sensitive indicator of functional disturbance. When cardiomyocytes are exposed to cytokine signaling or other inflammatory conditions, examining calcium-dependent activity can help reveal changes that may precede broader loss of contractility or viability. This provides a mechanistic link between immune activation and myocardial dysfunction.
Cytokine signaling can be examined as a direct cellular pathway through which inflammatory conditions affect the myocardium. In adult rat cardiomyocytes, researchers can evaluate whether such signaling alters contractile activity, cellular stress, or viability. These observations help distinguish inflammatory effects on cardiac performance from more general injury and clarify mechanisms of immune-mediated myocardial damage.
The experimental workflow begins with isolation from mature rats, followed by controlled culture conditions that permit assessment outside the whole animal. Maintaining this controlled setting allows researchers to expose the cells to defined environmental or inflammatory stimuli and then examine changes in structure, function, injury, or survival. The approach supports focused analysis of cardiac responses under experimentally varied conditions.
They are useful when investigators need to examine how inflammatory mediators or pathogen-associated effects act directly on cardiac muscle cells. The model supports studies of cytokine signaling, cellular stress, immune-mediated myocardial injury, and changes in contractility or viability. This ex vivo context helps connect immune or infection-related stimuli with cardiac dysfunction while limiting the complexity of whole-organism experiments.
Experiments can compare how controlled stimuli affect contractility, calcium-linked function, cellular stress, and viability. Together, these outcomes indicate whether a treatment primarily disrupts cardiac performance, damages cells, or produces both effects. In immunology and infection studies, the resulting evidence can clarify mechanisms of dysfunction and support evaluation of protective interventions aimed at preserving myocardial function.