Corrigendum to: Role of neuronal nitric oxide synthase in lipopolysaccharide-induced tumor necrosis factor-alpha expression in cardiomyocytes

Geoghegan-Morphet, Nicola; Burger, Dylan; Lu, Xiangru; Sathish, Venkatachalem; Peng, Tianqing; Sims, Stephen M.; Feng, Qingping

doi:10.1093/cvr/cvp041

Cited by 6 publications

(9 citation statements)

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“…Compared with adult mouse cardiomyocytes, neonatal mouse cardiomyocytes lack transverse tubules, which may have an advantage in voltage-clamp experiments (27). Neonatal mouse cardiomyocytes have been used as a model for ion channel expression, including for the Na ϩ channel Nav1.5 (39,44), Tand L-type Ca 2ϩ channels (17,21), the K ϩ channel Kv4.2 (18), and the pacemaker HCN channel (9). The study of WT and mutant ion channels in native cardiac myocyte models is important since ion channel mutations have been reported to function differently in native myocyte and HEK-293 cell expression systems (26).…”

Section: Discussionmentioning

confidence: 99%

Properties of WT and mutant hERG K⁺ channels expressed in neonatal mouse cardiomyocytes

Lin

Holzem

Anson

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Mutations in humanether-a-go-go-related gene 1 (hERG) are linked to long QT syndrome type 2 (LQT2). hERG encodes the pore-forming ␣-subunits that coassemble to form rapidly activating delayed rectifier K ϩ current in the heart. LQT2-linked missense mutations have been extensively studied in noncardiac heterologous expression systems, where biogenic (protein trafficking) and biophysical (gating and permeation) abnormalities have been postulated to underlie the loss-of-function phenotype associated with LQT2 channels. Little is known about the properties of LQT2-linked hERG channel proteins in native cardiomyocyte systems. In this study, we expressed wild-type (WT) hERG and three LQT2-linked mutations in neonatal mouse cardiomyocytes and studied their electrophysiological and biochemical properties. Compared with WT hERG channels, the LQT2 missense mutations G601S and N470D hERG exhibited altered protein trafficking and underwent pharmacological correction, and N470D hERG channels gated at more negative voltages. The ⌬Y475 hERG deletion mutation trafficked similar to WT hERG channels, gated at more negative voltages, and had rapid deactivation kinetics, and these properties were confirmed in both neonatal mouse cardiomyocyte and human embryonic kidney (HEK)-293 cell expression systems. Differences between the cardiomyocytes and HEK-293 cell expression systems were that hERG current densities were reduced 10-fold and deactivation kinetics were accelerated 1.5-to 2-fold in neonatal mouse cardiomyocytes. An important finding of this work is that pharmacological correction of trafficking-deficient LQT2 mutations, as a potential innovative approach to therapy, is possible in native cardiac tissue.

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Section: Discussionmentioning

confidence: 99%

Properties of WT and mutant hERG K⁺ channels expressed in neonatal mouse cardiomyocytes

Lin

Holzem

Anson

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…In addition, strychnine, a GLY receptor antagonist, given at a final concentration of 50 µmol/L, completely prevented the inhibitory effect of 2 mmol/L GLY on the 100 µg/mL LPS-induced elevation in ] c and in turn decreases TNFα production in macrophages [15] . Geoghegan-Morphet [18] et al demonstrated that 10 µg/mL LPS increased [Ca 2+ ] c and TNFα expression in cardiomyocytes and that pretreatment with the L-type calcium channel inhibitor verapamil partially decreased TNFα expression. This suggests that elevated [Ca 2+ ] c plays a role in TNFα production induced by LPS to a certain extent in cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

Glycine inhibits the LPS-induced increase in cytosolic Ca2+ concentration and TNFα production in cardiomyocytes by activating a glycine receptor

Wang

et al. 2009

Acta Pharmacol Sin

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Aim: Previous studies have demonstrated that glycine (GLY) markedly reduces lipopolysaccharide (LPS)-induced myocardial injury. However, the mechanism of this effect is still unclear. The present study investigated the effect of GLY on cytosolic calcium concentration ([Ca 2+ ] c ) and tumor necrosis factor-α (TNFα) production in cardiomyocytes exposed to LPS, as well as whether the glycine-gated chloride channel is involved in this process. Methods: Neonatal rat cardiomyocytes were isolated, and the [Ca 2+ ] c and TNFα levels were determined by using Fura-2 and a Quantikine enzyme-linked immunosorbent assay, respectively. The distribution of the GLY receptor and GLY-induced currents in cardiomyocytes were also investigated using immunocytochemistry and the whole-cell patch-clamp technique, respectively. Results: LPS at concentrations ranging from 10 ng/mL to 100 µg/mL significantly stimulated TNFα production. GLY did not inhibit TNFα production induced by LPS at concentrations below 10 ng/mL but did significantly decrease TNFα release stimulated by 100 µg/mL LPS and prevented an LPS-induced increase in [Ca 2+ ] c , which was reversed by strychnine, a glycine receptor antagonist. GLY did not block the isoproterenol-induced increase in [Ca 2+ ] c , but did prevent the potassium chloride-induced increase in [Ca 2+ ] c in cardiomyocytes. Strychnine reversed the inhibition of the KCl-stimulated elevation in [Ca 2+ ] c by GLY. In chloride-free buffer, GLY had no effect on the dipotassium hydrogen phosphate-induced increase in [Ca 2+ ] c . Furthermore, GLY receptor α 1 and β subunit-immunoreactive spots were observed in cardiomyocytes, and GLY-evoked currents were blocked by strychnine. Conclusion: Cardiomyocytes possess the glycine-gated chloride channel, through which GLY prevents the increase in [Ca 2+ ] c and inhibits the TNFα production induced by LPS at high doses in neonatal rat cardiomyocytes.

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“…Esta redução da DO 2 sem redução de sua demanda (VO 2 ) cria uma situação de rápida deterioração metabólica regional (43). Inicialmente há a diminuição da perfusão e oxigenação gastrintestinais seguida de perda da integridade da barreira mucosa com conseqüente translocação de bactérias e suas toxinas para a corrente sanguínea (9,33,(43)(44)(45)(46).…”

Section: Hipotensão Arterial Sistêmicaunclassified

“…No entanto, o lactato de maneira estática e como parâmetro único não é uma ferramenta confiável para traduzir a oxigenação tecidual, pois apesar do nível de lactato sérico ser utilizado como meio de se avaliar o quadro metabólico celular podemos encontrar alterações em seus níveis não relacionadas à hipóxia, como: o seu aumento após administração de fluidos que o contenha; a redução de seus níveis através do seu consumo como fonte energética e até mesmo seu aumento devido à falha em sua metabolização hepática e renal (12,14,32,39). Até mesmo a presença de endotoxinas em contato com as células pode reduzir ou inativar a utilização da enzima piruvatodesidrogenase no ciclo de Krebs, o que faria com que a célula passasse a produzir lactato sem que de fato haja uma situação de hipóxia (4,25,33).…”

Section: Hipotensão Arterial Sistêmicaunclassified

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Mecanismos de hipoperfusão tecidual na sepse experimental e efeitos da reposição volêmica com solução salina hipertônica-isoncótica e pentoxifilina

Dias¹

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Corrigendum to: Role of neuronal nitric oxide synthase in lipopolysaccharide-induced tumor necrosis factor-alpha expression in cardiomyocytes

Cited by 6 publications

References 0 publications

Properties of WT and mutant hERG K⁺ channels expressed in neonatal mouse cardiomyocytes

Properties of WT and mutant hERG K⁺ channels expressed in neonatal mouse cardiomyocytes

Glycine inhibits the LPS-induced increase in cytosolic Ca2+ concentration and TNFα production in cardiomyocytes by activating a glycine receptor

Mecanismos de hipoperfusão tecidual na sepse experimental e efeitos da reposição volêmica com solução salina hipertônica-isoncótica e pentoxifilina

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Corrigendum to: Role of neuronal nitric oxide synthase in lipopolysaccharide-induced tumor necrosis factor-alpha expression in cardiomyocytes

Cited by 6 publications

References 0 publications

Properties of WT and mutant hERG K+ channels expressed in neonatal mouse cardiomyocytes

Properties of WT and mutant hERG K+ channels expressed in neonatal mouse cardiomyocytes

Glycine inhibits the LPS-induced increase in cytosolic Ca2+ concentration and TNFα production in cardiomyocytes by activating a glycine receptor

Mecanismos de hipoperfusão tecidual na sepse experimental e efeitos da reposição volêmica com solução salina hipertônica-isoncótica e pentoxifilina

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Properties of WT and mutant hERG K⁺ channels expressed in neonatal mouse cardiomyocytes

Properties of WT and mutant hERG K⁺ channels expressed in neonatal mouse cardiomyocytes