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Rat Cardiac Myocytes (rat + cardiac_myocyte)
Selected AbstractsCell-to-cell cross-talk between mesenchymal stem cells and cardiomyocytes in co-cultureJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 5a 2008E. Y. Plotnikov Abstract The goals of the study were: (1) to explore the communication between human mesenchymal stem cells (MSC) and rat cardiac myocytes resulting in differentiation of the stem cells and, (2) to evaluate the role of mitochondria in it. Light and fluorescence microscopy as well as scanning electron microscopy revealed that after co-cultivation, cells formed intercellular contacts and transient exchange with cytosolic elements could be observed. The transport of cytosolic entity had no specific direction. Noticeably, mitochondria also could be transferred to the recipient cells in a unidirectional fashion (towards cardiomyocytes only). Transmission electron microscopy revealed significant variability in both the diameter of intercellular contacting tubes and their shape. Inside of these nanotubes mitochondria-resembling structures were identified. Moreover, after co-cultivation with cardiomyocytes, expression of human-specific myosin was revealed in MSC. Thus, we speculate that: (1) transport of intracellular elements to MSC possibly can determine the direction of their differentiation and, (2) mitochondria may be involved in the mechanism of the stem cell differentiation. It looks plausible that mitochondrial transfer to recipient cardiomyocytes may be involved in the mechanism of failed myocardium repair after stem cells transplantation. [source] Heme oxygenase-1 gene transfer inhibits angiotensin II-mediated rat cardiac myocyte apoptosis but not hypertrophy,JOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2006Roger S.Y. Foo Cardiac myocyte apoptosis underlies the pathophysiology of cardiomyopathy, and plays a critical role in the transition from myocardial hypertrophy to heart failure. Angiotensin II (Ang II) induces cardiac myocyte apoptosis and hypertrophy which contribute to heart failure possibly through enhanced oxidative stress; however, the mechanisms underlying the activation of both pathways and their interactions remain unclear. In the present study, we have investigated whether overexpression of the antioxidant protein heme oxygenase-1 (HO-1) protects against apoptosis and hypertrophy in cultured rat cardiac myocytes treated with Ang II. Our findings demonstrate that Ang II (100 nM, 24 h) alone upregulates HO-1 expression and induces both myocyte hypertrophy and apoptosis, assessed by measuring terminal deoxynucleotidyltransferase dUTP nick-end labelling (TUNEL) staining, caspase-3 activity and mitochondrial membrane potential. Ang II elicited apoptosis was augmented in the presence of tin protoporphyrin, an inhibitor of HO activity, while HO-1 gene transfer to myocytes attenuated Ang II-mediated apoptosis but not hypertrophy. Adenoviral overexpression of HO-1 was accompanied by a significant increase in Ang II induced phosphorylation of Akt, however, Ang II-mediated p38 mitogen activated protein kinase (MAPK) phosphorylation was attenuated. Inhibition of phosphotidylinositol-3-kinase enhanced myocyte apoptosis elicited by Ang II, however, p38MAPK inhibition had no effect, suggesting that overexpression of HO-1 protects myocytes via augmented Akt activation and not through modulation of p38MAPK activation. Our findings identify the signalling pathways by which HO-1 gene transfer protects against apoptosis and suggest that overexpression of HO-1 in cardiomyopathies may delay the transition from myocyte hypertrophy to heart failure. J. Cell. Physiol. 209: 1,7, 2006. © 2006 Wiley-Liss, Inc. [source] The effect of Polbax extract on lipofuscin accumulation in cultured neonatal rat cardiac myocytesPHYTOTHERAPY RESEARCH, Issue 2 2002Alexei Terman Abstract Polbax®, a water-soluble extract of fresh pollen grains and pistils, was tested for its ability to influence the accumulation of lipofuscin (age pigment) in cultured neonatal rat cardiac myocytes. Exposure for 3 weeks to Polbax at concentrations of 0.1, 1.0 or 10,mg/L decreased lipofuscin accumulation morphometrically assayed using laser scanning microscopy images (green excitation light) of formaldehyde-fixed cells, by 24%, 41% or 43%, respectively. Based on the knowledge that oxidative stress and iron-catalysed peroxidation play an important role in lipofuscinogenesis, we suggest that Polbax may slow lipofuscin formation due to antioxidant activities, perhaps involving intralysosomal dismutation of superoxide produced by autophagocytosed mitochondria and/or iron-chelation. Copyright © 2002 John Wiley & Sons, Ltd. [source] Electrophysiological Effects of the Anti-Cancer Drug Lapatinib on Cardiac RepolarizationBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2010Hyang-Ae Lee Although lapatinib is associated with a risk of QT prolongation, the effects of the drug on cellular cardiac electrical properties and on action potential duration (APD) have not been studied. To evaluate the potential effects of lapatinib on cardiac repolarization, we investigated its electrophysiological effects using a whole-cell patch,clamp technique in transiently transfected HEK293 cells expressing human ether-ŕ-go-go (hERG; to examine the rapidly activating delayed rectifier K+ current, IKr), KCNQ1/KCNE1 (to examine the slowly activating delayed rectifier K+ current, IKs), KCNJ2 (to examine the inwardly rectifying K+ current, IK1), or SCN5A (to examine the inward Na+ current, INa) and in rat cardiac myocytes (to examine the inward Ca2+ current, ICa). We also examined its effects on the APD at 90% (APD90) in isolated rabbit Purkinje fibres. In ion channel studies, lapatinib inhibited the hERG current in a concentration-dependent manner, with a half-maximum inhibition concentration (IC50) of 0.8 ± 0.09 ,m. In contrast, at concentrations up to 3 ,m, lapatinib did not significantly reduce the INa, IK1 or ICa amplitudes; at 3 ,m, it did slightly inhibit the IKs amplitude (by 19.4 ± 4.7%; p < 0.05). At 5 ,m, lapatinib induced prolongation of APD90 by 16.1% (p < 0.05). These results suggest that the APD90 -prolonging effect of lapatinib on rabbit Purkinje fibres is primarily a result of inhibition of the hERG current and IKs, but not INa, IK1 or ICa. [source] Perfusion seeding of channeled elastomeric scaffolds with myocytes and endothelial cells for cardiac tissue engineeringBIOTECHNOLOGY PROGRESS, Issue 2 2010Robert Maidhof Abstract The requirements for engineering clinically sized cardiac constructs include medium perfusion (to maintain cell viability throughout the construct volume) and the protection of cardiac myocytes from hydrodynamic shear. To reconcile these conflicting requirements, we proposed the use of porous elastomeric scaffolds with an array of channels providing conduits for medium perfusion, and sized to provide efficient transport of oxygen to the cells, by a combination of convective flow and molecular diffusion over short distances between the channels. In this study, we investigate the conditions for perfusion seeding of channeled constructs with myocytes and endothelial cells without the gel carrier we previously used to lock the cells within the scaffold pores. We first established the flow parameters for perfusion seeding of porous elastomer scaffolds using the C2C12 myoblast line, and determined that a linear perfusion velocity of 1.0 mm/s resulted in seeding efficiency of 87% ± 26% within 2 hours. When applied to seeding of channeled scaffolds with neonatal rat cardiac myocytes, these conditions also resulted in high efficiency (77.2% ± 23.7%) of cell seeding. Uniform spatial cell distributions were obtained when scaffolds were stacked on top of one another in perfusion cartridges, effectively closing off the channels during perfusion seeding. Perfusion seeding of single scaffolds resulted in preferential cell attachment at the channel surfaces, and was employed for seeding scaffolds with rat aortic endothelial cells. We thus propose that these techniques can be utilized to engineer thick and compact cardiac constructs with parallel channels lined with endothelial cells. © 2010 American Institute of Chemical Engineers Biotechnol. 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