Neonatal rat ventricular myocyte

Darrow BJ, Laing JG, Lampe PD, Saffitz JE, Beyer EC Expression of multiple connexins in cultured neonatal rat ventricular myocytes. Circ Res 1995 76 381-387. 

Karliner JS, Kagiya T, Simpson PC. 1990. Effects of pertussis toxin on alpha 1-agonist-mediated phosphatidylinositide turnover and myocardial cell hypertrophy I neonatal rat ventricular myocytes. Experientia (Basel) 46 81-84. 

Strait, J.B., Martin, J.L., Bayer, A., Mestril, R., Eble, D.M., and Samarel, A.M. 2001. Role of protein kinase C-e in hypertrophy of cultured neonatal rat ventricular myocytes. Am. J. Physiol. 280 H756-H766. 

Rajapurohitam, V., Gan, X. T., Kirshenbaum, L. A., and Karmazyn, M. 2003. The obesity-associated peptide leptin induces hypertrophy in neonatal rat ventricular myocytes. Circ. Res. 93 277-279. 

Kanaya et al. (1998) Compared myocardial depression by sevoflurane, isofluorane, or halothane in cultured neonatal rat ventricular myocytes. Changes in beating rate and amplitude during exposure to the anesthetics were measured. 

Lamorte VJ, Thorburn J, Absher D, et al. Gq-Dependent and Ras-dependent pathways mediate hypertrophy of neonatal rat ventricular myocytes following a,-adrenergic stimulation. J Biol Chem 1994 269 13,490-13,496. 

Post GR, Goldstein D, Thuerauf DJ, Glembotski CC, Brown JH. Dissociation of p44 and p42 mitogen-activated protein kinase activation from receptor-induced hypertrophy in neonatal rat ventricular myocytes. J Biol Chem 1996 271 8452-8457. 

Fuller SJ, Gillespie-Brown J, Sugden PH. Oncogenic src, raf and ras stimulate a hypertrophic pattern of gene expression and increase cell size in neonatal rat ventricular myocytes. J Biol Chem 1998 273 18,146-18,152. 

Heidkamp MC, Bayer AL, Martin JL, Samarel AM. 2001. Differential activation of mitogen-activated protein kinase cascades and apoptosis by protein kinase C e and S in neonatal rat ventricular myocytes. Circ. Res. 89 882-90... 

GJ opening may also contribute to cardioprotection. Survival signals can be transferred from one cell to another. In fact, cell to cell interaction through GJ has been described to prevent apoptosis in neonatal rat ventricular myocytes.26 The intensity of the stimulus is likely to determine the beneficial or detrimental role of GJ communication. See also chapter 4. 

Endothelin-1 is a potent vasoconstrictor peptide derived from endothelial cells.100 Its physiological function is mediated by two receptors the ET-A and ET-B. Table 1. Figure 11. ET-A and ET-B receptors are located in vascular smooth muscle and their activation causes vasoconstriction, whereas ET-B receptor is also located in the endothelium and its activation results in vasodilation by increasing nitric oxide or prostacyclin. Endothelin is released following myocardial ischemia and reperfusion. Endothelin reduces infarct size in a perfused rat heart model of ischemia and reperfusion through activation of protein kinase C and KATp channel.101 Furthermore, in neonatal rat ventricular myocytes, endothelin is shown to activate the calcineurin-NFAT (nuclear factor of activated cells) pathways and enhance the expression of Bcl-2.102 However, endogenous blockade of endothelin at the level of the ET-A receptor reduced infarct size in a pig model of coronary occlusion and reperfusion.103... 

K. Yasui, K. Kada, M. Hozo, J.K. Lee, K. Kamiya, J. Toyama, T. Opthof and I. Kodama, Ccll-to-ccll interaction prevents cell death in cultured neonatal rat ventricular myocytes, Cardiovasc. Res. 48,68-76 (2000). 

Xiao YF, Gomez AM, Morgan JP, Lederer WJ, Leaf A. Suppression of voltage-gated L-type Ca currents by polyunsaturated fatty acids in adult and neonatal rat ventricular myocytes. Proc Natl Acad Sci USA 1997 94 4182-4187. 

Many studies have shown that chronic a,-adrenoceptor activation can induce cardiac hypertrophy. Studies in cells transfected with the recombinant a, adrenoceptors show that all three subtypes can increase levels of early gene markers of cellular proliferation (Garcia-Sainz et al., 1998). Use of subtype selective antagonists indicated that phenyel-phrine-induced hypertrophy in neonatal rat ventricular myocytes was mediated by the q , subtype (Knowlton et al.,... 

Movie A video showing the hybrid culture grown on top of the micro-electrode array plate. The image is shown at a high magnification (x40). Note the synchronous contractions of the hES cell-derived cardiomyocyte tissue (cell cluster on the right side of the image) and the neonatal rat ventricular myocyte monolayer. 

Barac Y.D., Zeevi-Levin N., Yaniv G., Reiter L, Mihnan F., Shilkrut M., Coleman R., Abassi Z., Binah O. The 1,4,5-inositol trisphosphate pathway is a key component in Fas-mediated hypertrophy in neonatal rat ventricular myocytes. Cardiovasc. Res. 68 (2005) 75-86. 

Suzuki H, Tomida A, Tsuruo T. Dephosphorylated hypoxia-inducible factor lot as a mediator of p53-dependent apoptosis during hypoxia. Oncogene 2001 20 5779-5788. Goldberg M, Zhang HL, Steinberg SE Hypoxia alters the subcellular distribution of protein kinase C isoforms in neonatal rat ventricular myocytes. J Clin Invest 1997 99 55-61. 

Jacot, J.G., A.D. Mcculloch, and J.H. Omens. 2008. Substrate stiffness affects the functional maturation of neonatal rat ventricular myocytes. Biophysical Journal 95(7) 3479-87. 

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