Disease relevance of Myoblasts, Cardiac

• In cultured rat cardiac myoblasts (H9C2 cells), EPO also reduced the increase in DNA fragmentation caused by either serum deprivation (simulated ischemia) or hydrogen peroxide (oxidative stress) [1].
• Endogenous production and exogenous exposure to nitric oxide augment doxorubicin cytotoxicity for breast cancer cells but not cardiac myoblasts [2].
• Modulation of interleukin-6 in cardiac myoblasts during endotoxemia [3].

High impact information on Myoblasts, Cardiac

• Mechanism of hydrogen peroxide and hydroxyl free radical-induced intracellular acidification in cultured rat cardiac myoblasts [4].
• In this study, we examined the impact of inhibition of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase with simvastatin on the expression of inducible nitric-oxide synthase (iNOS) in embryonic cardiac myoblasts stimulated with the proinflammatory cytokines, interleukin-1 or tumor necrosis factor [5].
• Simvastatin attenuates expression of cytokine-inducible nitric-oxide synthase in embryonic cardiac myoblasts [5].
• Diabetic mice produced by streptozotocin and H9c2 cardiac myoblast cells exposed to high levels of glucose were used [6].
• Regulation of cardiolipin biosynthesis in H9c2 cardiac myoblasts by cytidine 5'-triphosphate [7].

Chemical compound and disease context of Myoblasts, Cardiac

• Activation of glucose transport during simulated ischemia in H9c2 cardiac myoblasts is mediated by protein kinase C isoforms [8].

Biological context of Myoblasts, Cardiac

• Signal transduction of arginine vasopressin-induced arachidonic acid release in H9c2 cardiac myoblasts: role of Ca2+ and the protein kinase C-dependent activation of p42 mitogen-activated protein kinase [9].
• To better understand how MAPKAP kinase 2 is regulated in myocardium, cultured rat cardiac myoblast (H9c2) cells were stimulated with heat shock, H2O2-induced oxidative stress, or phorbol ester (PMA) [10].
• Insulin-like growth factor-1 protects H9c2 cardiac myoblasts from oxidative stress-induced apoptosis via phosphatidylinositol 3-kinase and extracellular signal-regulated kinase pathways [11].
• An investigation of PDGF C mRNA and protein expression revealed that during mouse fetal development, PDGF C was expressed in the mesonephric mesenchyme, prefusion skeletal muscle, cardiac myoblasts, and in visceral and vascular smooth muscle, whereas in adult human tissues expression was largely restricted to smooth muscle [12].

Anatomical context of Myoblasts, Cardiac

• Our findings indicate that the cellular CTP level may regulate cardiolipin biosynthesis in H9c2 cardiac myoblasts and support the notion that the cellular CTP level may be a universal signal/switch for all phospholipid biosynthesis in eukaryotic cells [7].
• The most intense activity of TGase C was observed in some cardiac myoblasts infiltrating into endocardial mesenchyme at 6-7 weeks after fertilization [13].
• The mechanism of the chloroquine-mediated modulation of new cardiolipin biosynthesis in isolated rat liver hepatocytes and H9c2 cardiac myoblast cells was addressed in this study [14].
• We examined the role of Ca(2+)-dependent signal in caveolin- mediated growth inhibition using a rat cardiac myoblast cell line (H9C2), in which the expression of caveolin- 3, the muscle specific subtype, can be induced using the LacSwitch system [15].

Associations of Myoblasts, Cardiac with chemical compounds

• The regulation of cardiolipin biosynthesis by CTP in H9c2 cardiac myoblasts was investigated [7].
• Rat cardiac myoblasts (H9c2 cells) were preincubated with the PARS inhibitors, 3-AB. nicotinamide (Nic) or 1,5-dihydroxyisoquinoline (ISO) or the inactive analogues 3-ABA or nicotinic acid (NicA) prior to exposure with hydrogen peroxide (1 mM) [16].
• The PARS inhibitors 3-aminobenzamide (3 mM), 1,5-dehydroxyisoquinoline (300 microM) or nicotinamide (3 mM) attenuated the cell injury and death as well as the increase in PARS activity caused by hydrogen peroxide (3 mM; 4 h for cell injury/death, 60 min for PARS activity) in human cardiac myoblasts [17].
• The iron chelator deferoxamine (1-10 mM) caused a concentration-dependent reduction in the cell injury and death caused by hydrogen peroxide in these human cardiac myoblasts [17].
• Protection by inhibition of poly (ADP-ribose) synthetase against oxidant injury in cardiac myoblasts In vitro [18].

Gene context of Myoblasts, Cardiac

• As in vitro, the antiapoptosis effect of VEGF(165), Ang1 and VEGF(165)+Ang1 on cardiac myoblasts was observed, which seemed to be related with the activation of phosphatidylinositol-3 kinase and Bcl-2 pathways [19].
• Role of phospholipase C-gamma1 in insulin-like growth factor I-induced muscle differentiation of H9c2 cardiac myoblasts [20].
• CONCLUSIONS: In cardiac myoblasts, IL-6 is either enhanced or reduced depending on interactions between LPS and cytokine challenge [3].
• Our findings suggest that caveolin exhibits growth inhibition in a Ca(2+)-dependent manner, most likely through PKC, in cardiac myoblasts [15].
• Caveolin-3 inhibits growth signal in cardiac myoblasts in a Ca(2+)-dependent manner [15].

References