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Cardiac myocyte differentiation reported thus far is from iPS cells generated from mouse and human fibroblasts. However, there is no article on the generation of iPS cells from cardiac ventricular specific cell types such as H9c2 cells. Therefore, whether transduced H9c2 cells, originally isolated from embryonic cardiac ventricular tissue, will be able to(More)
Oxidative stress is involved in mitochondrial apoptosis, and plays a critical role in ischemic heart disease and cardiac failure. Exposure of cardiomyocytes to H(2)O(2) leads to oxidative stress and mitochondrial dysfunction. In this study, we investigated the temporal order of mitochondrial-related events in the neonatal rat cardiomyocyte response to(More)
p53 is an important regulator of cell growth and apoptosis and its activity is regulated by phosphorylation. Accordingly, in neonatal rat cardiomyocytes we examined the involvement of p53 in H2O2-induced apoptosis. Treatment with 50–100 μM H2O2 markedly induced apoptosis in cardiomyocytes, as assessed by gel electrophoresis of genomic DNA. To examine(More)
Recent studies suggest that Klf5 is required to maintain embryonic stem (ES) cells in an undifferentiated state. However, whether Klf5 can be inactivated by novel fusion technology of zinc finger nucleases (ZFN) has never before been examined. Therefore, we used ZFN technology to target the Klf5 gene in mouse ES cells, and examined the effects of the Klf5(More)
Calyculin A was used to examine the importance of phosphatases in the modulation of cardiac contractile magnitude in the absence of any neural or humoral stimulation. Protein phosphatase (PP)1 and PP2A activity, twitch contractions, intracellular Ca(2+) concentration ([Ca(2+)](i)) transients, action potentials, membrane currents, and myofilament Ca(2+)(More)
BACKGROUND Heme oxygenase-1 (HO-1) is a stress protein and the rate-limiting enzyme in heme degradation. We sought to examine the notion that protein kinases and phosphatases through phosphorylation and dephosphorylation modulate the HO-1 expression in cardiomyocytes under hypoxic conditions. METHODS AND RESULTS Exposure of neonatal rat cardiomyocytes to(More)
Although adenoviral SERCA gene transfer improves cardiac function in the failing heart, there is controversy regarding the cytotoxic effect of such overexpression. We sought to examine the effect of SERCA1 overexpression on neonatal (NRCMs) and adult rat cardiomyocytes (ARCMs). Cultured NRCMs and ARCMs were infected with adenoviral vector expressing EGFP(More)
Activation of the vacuolar proton ATPase (VPATPase) has been implicated in the prevention of apoptosis in neutrophils and adult cardiac myocytes. To determine the role of the VPATPase in apoptosis of cardiac myocytes, we used a potent and specific inhibitor of the VPATPase, bafilomycin A1. Bafilomycin A1 alone caused increased DNA laddering of genomic DNA(More)
Heme oxygenase-1 (HO-1), a rate-limiting enzyme in heme catabolism, has been shown to play a regulatory role in the expression of plasminogen activator inhibitor-1 (PAI-1), a risk factor for vascular disease. Accordingly, we examined the effect of protoporphyrins, both HO inhibitors and activators, on PAI-1 expression in human vascular smooth muscle cells(More)
The possibility that a significant fraction of cardiac myocyte loss in various disease states occurs through apoptosis has elicited considerable attention in recent years. Evidence from human studies as well as in vitro and animal models of disease has shown that cardiac myocyte apoptosis can be induced by a variety of stimuli and in a number of disease(More)
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