Cell, animal myocyte

Anyone eating a steak or a slice carved from roast beef knows that meat is fibrous in texture. These fibers, 20 to 100 fj.m in diameter and very long, are the multinucleate muscle cells of which skeletal muscles are composed (Fig. 1 A, B). Such fibers in the light microscope appear cross-striated and the muscles from which they are derived are known as striated muscles. The term striated also covers the muscles in animal hearts (Fig. 1C), but here the cells (the myocytes) are much shorter, they contain a single nucleus, and they are linked end to end by special structures known as... 

The effect of cellular GSH depletion on /wa/K has also been studied using this model. Guinea-pig ventricular myocytes prepared from DEM-treated animals have been used to determine the effect of glutathione depletion on /xa/K- Myocytes prepared from DEM-treated animals showed a similar profile of glutathione content modification to that previously described in experiments using sarcolemmal homogenates. GSH levels in DEM-treated were reduced from a control value of 0.2 0.04 to 0.02 0.01 nmol/1 X10 cells. Jni/k at 0 mV was reduced from a control value of 1.1 0.12 to... 

Studies in various animal models and in human hearts suggest that apoptosis does occur in ischemia/reperfusion injury of the heart, though the relative contribution of apoptosis in comparison with necrosis to cell loss in ischemia/ reperfusion injury is still controversial. Cardiomyocyte apoptosis was first reported by Gottlieb et al. [107], who studied the ischemia/reperfusion in rabbit hearts and found the hallmark of apoptosis in ischemic/reperfused hearts but not in the normal or ischemic-only rabbit hearts. Identification of apoptosis was based on the presence of fragmented DNA in electrophoretic gels, on in situ nick end-labeling assays, and on electron microscopy. They concluded that apoptosis may be a specific feature of reperfusion injury in cardiac myocytes. Subsequent studies have shown that apoptosis probably occurs both in ischemia and reperfusion [108], It appears that apoptosis is more prominent after ischemia followed by reperfusion than after ischemia alone [109, 110],... 

PrARs couple to the stimulatory Gs protein in both adult and neonatal myocytes, which leads to activation of adenylyl cyclase and production of cAMP (Fig. 1). In adult myocytes, the cAMP-dependent PKA phosphorylates various substrates, including the L-type Ca2+ channel, which increases Ca2+ entry into cells. PKA-mediated phosphorylation of phospholamban accelerates Ca2+ sequestration into the sarcoplasmic reticulum, resulting in accelerated cardiac relaxation (17). PKA-mediated phosphorylation of troponin I and C proteins reduces myofilament sensitivity to Ca2+ (17). The ryanodine receptor is also a substrate for PKA ryanodine receptor hyperphosphorylation has been observed in the failing human heart and in animal models of heart failure (58,59). Both in vivo and in vitro assays showed that the prAR plays the predominant role in modulating the rate and force of myocyte contraction in the mouse (24,30,55). 

A possible novel therapeutic strategy for heart failure following myocardial infarction may be to increase the number of functional myocytes within the diseased area by the implantation of exogenous myogenic cells. Early studies used neonatal rat cardiomyocytes for transplantation, as these cells have cardiac phenotype and still retain some proliferation capacity [2-4]. Fetal cardiomyocyte cell grafts showed the formation of cell-to-cell contacts, complete with gap junction proteins [4]. Moreover, cultured human fetal cardiomyocytes were shown to survive, and fetal rat cardiomyocytes were shown to be present in the infarcted rats hearts for up to 6 months after transplantation [5]. Further studies in animal models of myocardial infarction showed that grafting of cardiomyocytes from fetal and neonatal sources was asso-... 

Ionic currents measured in isolated animal or human cardiac myocytes (or cardiomyocytes), cultured cardiac cell lines, or heterologous expression systans for cloned human ion channels... 

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