Phospholemman (PLM) regulates cardiac Na(+)/Ca(2+) exchanger (NCX1) and Na(+)-K(+)-ATPase in cardiac myocytes. PLM, when phosphorylated at Ser(68), disinhibits Na(+)-K(+)-ATPase but inhibits NCX1. PLM regulates cardiac contractility by modulating Na(+)-K(+)-ATPase and/or NCX1. In this study, we first demonstrated that adult mouse cardiac myocytes cultured for 48 h had normal surface membrane ar...

In this study we present a novel computational model for unprecedented simulations of the whole cardiac electrophysiology. According to heterogeneous electrophysiologic properties heart, geometry is decomposed into set coupled conductive media having different topology and electrical conductivities: (i) network slender bundles comprising fast conduction atrial network, AV–node ventricular bundl...

Previous studies showed increased phospholemman (PLM) mRNA after myocardial infarction (MI) in rats (Sehl PD, Tai JTN, Hillan KJ, Brown LA, Goddard A, Yang R, Jin H, and Lowe DG. Circulation 101: 1990-1999, 2000). We tested the hypothesis that, in normal adult rat cardiac myocytes, PLM overexpression alters contractile function and cytosolic Ca(2+) concentration ([Ca(2+)](i)) homeostasis in a m...

The aim of this study was to investigate the importance of Toll-like receptor 4 (TLR4) signaling on cardiac myocytes versus immune cells in lipopolysaccharide (LPS)-induced cardiac dysfunction. Cardiac myocytes isolated from LPS-treated C57Bl/6 mice showed reduced shortening and calcium transients as compared with myocytes from untreated mice. In addition, LPS-treated C57Bl/6 mice showed impair...

Current cellular models of ischemic preconditioning (IPC) rely on inducing preconditioning in vitro and may not accurately represent complex pathways triggered by IPC in the intact heart. Here, we show that it is possible to precondition the intact heart and to subsequently isolate individual ventricular myocytes that retain the protection triggered by IPC. Myocytes isolated from Langendorff-pe...

The functional significance of the developmental transition from slow skeletal troponin I (ssTnI) to cardiac TnI (cTnI) isoform expression in cardiac myocytes remains unclear. We show here the effects of adenovirus-mediated ssTnI gene transfer on myofilament structure and function in adult cardiac myocytes in primary culture. Gene transfer resulted in the rapid, uniform, and nearly complete rep...

We have raised a mouse monoclonal antibody that reacts specifically with the myocytes of the sinoatrial node of the bovine heart. By use of this antibody (445-6E10) and antibodies against the gap junction protein connexin43, the periphery of the sinoatrial node and the distribution of gap junctions in the nodal region were studied. The reaction patterns of 445-6E10 and anti-connexin43 are exact...

Mitarai, Sayaka, Thomas D. Reed, and Atsuko Yatani. Changes in ionic currents and b-adrenergic receptor signaling in hypertrophied myocytes overexpressing Gaq. Am J Physiol Heart Circ Physiol 279: H139–H148, 2000.—Transgenic overexpression of Gaq causes cardiac hypertrophy and depressed contractile responses to b-adrenergic receptor agonists. The electrophysiological basis of the altered myocar...

Recently, we defined an alpha1A-adrenergic receptor-ERK (alpha1A-AR-ERK) survival signaling pathway in adult cardiac myocytes. Previous studies in neonatal cardiac myocytes indicated that the cardiac-specific transcription factor GATA4 is a downstream mediator of alpha1-ERK signaling and that phosphorylation of GATA4 by ERK increases DNA binding and transcriptional activity. Therefore, we exami...

Introduced several decades ago, the dogma persists that cardiac myocytes are terminally differentiated cells and that division of muscle cells is impossible in the adult heart. More recently, nuclear mitotic divisions in myocytes occasionally were seen, but those observations were challenged on the assumption that the rate of cell proliferation was inconsequential for actual tissue regeneration...