Victor Forge
The cardiac muscle, also known as the myocardium, is one of three major categories of muscles in the human body. It is responsible for the contractility of the heart and, therefore, the pumping action. The primary function of the cardiac muscle is to pump blood into circulation by generating enough force. Cardiac muscle cells, also known as cardiomyocytes, are striated, branched, and contain many mitochondria. They are under involuntary control. The mitotic activity of these highly differentiated cells is tightly suppressed.
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What You'll Learn
Cardiac myocytes and mitosis in rats
Cardiac myocytes proliferate rapidly during fetal life but exit the cell cycle soon after birth in mammals. Cardiac myocytes in rat hearts lose their ability to undergo cytokinesis between days 3 and 4, resulting in the formation of binucleated myocytes. This process of nuclear division without cellular division is a specific form of endoreduplication known as acytokinetic mitosis. In mitotic myocytes from both 2- and 4-day-old rats, actin disassembled in prometaphase, concentrated in the equator of the mitotic spindle in late anaphase, and formed a circumferential intensely staining band in early telophase.
Sarcomeric myosin and myomesin were only partially disassembled in mitotic myocytes from both 2- and 4-day-old rats. The actin-myosin contractile ring was formed during the binucleation process of cardiac myocytes. In addition, molecules involved in the latter stages of cytokinesis may be responsible for incomplete cytokinesis during binucleation. Interestingly, these cardiomyocytes still assembled an actomyosin contractile ring in culture, but abscission no longer took place.
The extent of adult cardiac myocyte proliferation is controversial, with species-specific differences observed. For instance, adult ventricular myocytes were previously believed to be terminally differentiated cells incapable of division. However, a recent study revealed that mitotic division occurs in both healthy and diseased hearts. Acute myocardial infarction can lead to upregulation of the IGF-1 autocrine system, DNA replication, and nuclear mitotic division in the remaining viable cardiac myocytes.
Isolated cardiac muscle cells grown in vitro have been studied for their ability to contract spontaneously and maintain myofibrillar organisation. It was found that the cessation of beating and disorganisation of myofibrils are not prerequisites for the division of cardiac muscle cells. Some sarcomeres within isolated cardiomyocytes persist throughout mitosis, and most myosin filaments remain bundled with myomesin in mitotic myocytes.
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Myofibril organisation and mitosis in cultured cardiac muscle cells
The interrelations between the proliferation and differentiation processes during cardiac myogenesis and regeneration have been a subject of interest for investigators for over a century. Myofibril organisation and mitosis in cultured cardiac muscle cells have been studied to understand the complex proliferative behaviour of cardiac-muscle cells in normal myogenesis and regeneration and its dependence on the differentiative properties of these cells.
In one study, enzymatically isolated cardiac myocytes from 2- and 4-day-old rats were used to investigate the organisation and distribution of actin, myomesin, and myosin. The actin–myosin contractile ring was formed in mitotic myocytes from both 2- and 4-day-old animals, with some differences in the organisation and distribution of actin, myosin, and myomesin. In mitotic myocytes from both age groups, actin disassembled in prometaphase, concentrated in the equator of the mitotic spindle in late anaphase, and formed a circumferential band in early telophase. Cytoplasmic myosin was evenly distributed as small spots and associated with the cell membrane from interphase to early anaphase, becoming more concentrated in the cortical membrane in the equator region in late anaphase, and forming a ring-like structure in early telophase. Sarcomeric myosin and myomesin were only partially disassembled in mitotic myocytes from both age groups, indicating that the actin–myosin contractile ring forms during the binucleation process of cardiac myocytes.
In another study, isolated cardiac muscle cells grown in vitro were examined for their ability to contract spontaneously and maintain myofibrillar organisation during division. These cells did not round up to undergo mitosis but instead divided by pinching themselves in two in a selected area, minimising disturbance to cell attachment sites and myofibrils. This study also found that cessation of beating and disorganisation of myofibrils are not prerequisites for the division of cardiac muscle cells.
Investigations into DNA synthesis, mitosis, and differentiation in cardiac myogenesis have revealed that muscle cells in embryonic chick hearts differ in morphology, including the content of cross-striated myofibrils, their ability to synthesise DNA and undergo mitosis, and their frequency of contraction. Contracting cells containing cross-striated myofibrils can undergo mitosis in vitro, resulting in spontaneously beating daughter cells containing cytoplasmic fibrils.
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Myocyte nuclear mitotic division in dogs
Cardiac muscle, also known as myocardium, is one of the three major categories of muscles in the human body. It is responsible for the contractility of the heart and, consequently, the pumping action. Cardiac muscle cells, or cardiomyocytes, are striated, branched, and contain many mitochondria. Each cardiomyocyte contains a single, centrally located nucleus surrounded by a cell membrane called the sarcolemma.
Myocyte nuclear mitotic division and programmed myocyte cell death are characteristics of cardiac myopathy induced by rapid ventricular pacing in dogs. This phenomenon is accompanied by DNA fragmentation and apoptotic cell death, which contribute to wall thinning and chamber dilation. The activation of cyclins and cyclin-dependent kinases (CDKs) is linked to myocyte proliferation and preservation of telomeric length in the failing heart. However, the inability of myocytes to re-enter the cell cycle in vitro may be due to a block in the activation of cyclins and CDKs. This inhibition may not occur in vivo, as myocyte proliferation is present in the failing heart.
In vivo studies in dogs have shown that ventricular pacing induces cardiac failure, leading to significant changes in the quantity and activity of cyclins and CDKs. For example, cyclin D2 and its associated kinase activity increased 7-fold and 3-fold, respectively. Similarly, cyclin A and cyclin B quantities and activities were elevated by 4-fold. The cell-division control protein 2 (cdc2) and cyclin-dependent kinase 2 (cdk2) activities also increased substantially, by 8-fold and 5-fold, respectively.
Understanding the mechanisms that control cardiac myocyte cell cycles is essential for developing reagents or procedures to initiate the repair or regeneration of the adult myocardium following injury. By reverting cardiac muscle cells to their biochemically active state during early fetal growth, when they actively divided and proliferated, it may be possible to design interventions that promote cardiac muscle regeneration.
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Mitosis in neonatal myocytes
Cardiac muscle cells, also known as cardiomyocytes, are striated, branched, and contain many mitochondria. They are under involuntary control and are responsible for the contractility of the heart, which is termed cardiac output.
Cardiac myocytes proliferate rapidly during fetal life, but this proliferation ceases soon after birth. Before exiting the cell cycle, cardiomyocytes undergo an additional round of DNA synthesis and nuclear mitosis without cytokinesis, resulting in binucleated cardiomyocytes. This process is known as acytokinetic mitosis and occurs during early fetal growth when cardiac muscle cells are actively dividing and proliferating.
In neonatal myocytes, actin gets disassembled during the early stages of mitosis. The actin–myosin contractile ring is formed in mitotic myocytes, and changes in the organization and distribution of actin, myosin, and myomesin occur. These changes are similar in 2- and 4-day-old rats, except that longitudinal actin filaments are present in the cytoplasm of 4-day-old rats. During mitosis, actin disassembles in prometaphase, concentrates at the equator of the mitotic spindle in late anaphase, and forms a circumferential band in early telophase.
The study of mitosis in neonatal myocytes can provide insights into cardiac regeneration and repair. For example, understanding the mechanisms that control the cardiac myocyte cell cycle could allow for the development of reagents or procedures to initiate repair or regeneration of the adult myocardium following injury. Additionally, cardiac injury in newborn mammalian hearts has been found to accelerate cardiomyocyte terminal differentiation, with apical resection promoting a transient burst in cardiomyocyte cell cycle activity.
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Mitosis in adult cardiac myocytes
Mitosis is the process by which cells divide to produce two identical daughter cells, each containing the same number of chromosomes and genetic content as their parent cell. Cardiac myocytes, also known as cardiomyocytes, are the cells that make up the cardiac muscle, which is responsible for the heart's contractility and pumping action.
It was previously believed that adult ventricular myocytes were terminally differentiated cells, incapable of division. However, recent studies have challenged this notion by providing evidence of mitotic division in both healthy and diseased hearts. This discovery has significant implications for understanding and potentially treating cardiac injuries and diseases.
While mitosis does occur in adult cardiac myocytes, it is important to note that the regenerative capacity of the heart is limited. Investigators generally agree that adult cardiomyocytes have a very limited potential for self-renewal, which is often inadequate for repairing the heart after a significant injury. This inability of the adult mammalian myocardium to reactivate the cell cycle is a primary limiting factor in restoring function to a damaged heart.
The mechanisms that control the cardiac myocyte cell cycle are not yet fully understood. However, some studies have suggested that cardiac myocytes can enter the S phase, the period during which DNA replication occurs. Despite this, more than half of these cells arrest at either the entry to mitosis or during cytokinesis, the final step of cell division where the cytoplasm is partitioned and separated between the daughter cells.
Further research is needed to fully comprehend the intricacies of cardiac myocyte division and its potential applications in regenerative medicine. Understanding the mechanisms that regulate the cardiac myocyte cell cycle could lead to the development of reagents or procedures that initiate repair or regeneration of the adult myocardium following injury.
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Frequently asked questions
Cardiac muscle cells (cardiomyocytes) are mitotic during early fetal growth, but mitotic activity is suppressed in adult cardiac muscles.
Understanding the mechanisms that control the cardiac myocyte cell cycle would allow scientists to design reagents or procedures to initiate the repair or regeneration of the adult myocardium following injury.
It is not clear what happens to the myofibrillar apparatus during cardiac muscle cell division. However, there are indications of partial disassembly of myofibrils, particularly the Z-disks.
