Impairment of HERG K+ Channel Function by Tumor Necrosis Factor-α

Wang, Jingxiong; Wang, Huizhen; Zhang, Yiqiang; Gao, Huanhuan; Nattel, Stanley; Wang, Zhiguo

doi:10.1074/jbc.c400025200

Cited by 136 publications

(85 citation statements)

References 25 publications

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“…(a) (b) It is evident that the greatest efficiency provided by the green mussels shell desulfurizer was comparable to the slaked lime one as reported by Wang et al [24,25]; that SO 2 emissions were reduced by 75-95% during the combustion of bio-briquettes as compared to low rank coal. Their bio-briquettes were prepared under high pressure by blending the low rank coal (70-85 wt%) and biomass (15-30 wt%) at Ca/S ratio 1.5-2.0.…”

Section: Use Of Green Mussel Shell As a Desulfurizer In The Blendingsupporting

confidence: 55%

Use of Green Mussel Shell as a Desulfurizer in the Blending of Low Rank Coal-Biomass Briquette Combustion

Mahidin¹,

Gani²,

Hani³

et al. 2016

MST

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Calcium oxide-based material is available abundantly and naturally. A potential resource of that material comes from marine mollusk shell such as clams, scallops, mussels, oysters, winkles and nerites. The CaO-based material has exhibited a good performance as the desulfurizer or adsorbent in coal combustion in order to reduce SO 2 emission. In this study, pulverized green mussel shell, without calcination, was utilized as the desulfurizer in the briquette produced from a mixture of low rank coal and palm kernel shell (PKS), also known as bio-briquette. The ratio of coal to PKS in the briquette was 90:10 (wt/wt). The influence of green mussel shell contents and combustion temperature were examined to prove the possible use of that material as a desulfurizer. The ratio of Ca to S (Ca = calcium content in desulfurizer; S = sulfur content in briquette) were fixed at 1:1, 1.25:1, 1.5:1, 1.75:1, and 2:1 (mole/mole). The burning (or desulfurization) temperature range was 300-500 °C; the reaction time was 720 seconds and the air flow rate was 1.2 L/min. The results showed that green mussel shell can be introduced as a desulfurizer in coal briquette or bio-briquette combustions. The desulfurization process using that desulfurizer exhibited the first order reaction and the highest average efficiency of 84.5%. AbstrakPemanfaatan Cangkang Kerang Hijau sebagai Desulfurizer dalam Pembakaran Briket Campuran Batubara Peringkat Rendah-Biomassa. Bahan alam berbasis kalsium oksida (CaO) tersedia secara melimpah. Salah satu sumberdaya yang potensial dari bahan alam tersebut berasal dari cangkang moluska laut antara lain kerang, simping (kerang kampak), remis, tiram, keong dan siput (siput terompet). Bahan berbasis CaO tersebut memperlihatkan unjuk kerja yang baik sebagai desulfurizer atau adsorben dalam pembakaran batubara untuk mereduksi emisi SO2. Dalam kajian ini, serbuk cangkang kerang hijau, tanpa kalsinasi, digunakan sebagai desulfurizer dalam produksi briket dari campuran batubara peringkat rendah dan cangkang kelapa sawit (CKS), yang juga dikenal dengan bio-briket. Rasio batubara terhadap CKS dalam briket adalah 90:10 (dalam berat). Pengaruh kandungan cangkang kerang hijau dan temperatur pembakaran dikaji dalam rangka untuk membuktikan kemungkinan pemanfaatan bahan tersebut sebagai desulfurizer. Perbandingan Ca terhadap S (Ca = kandungan kalsium dalam desulfurizer; S = kandungan sulfur dalam briket) ditetapkan sebesar 1:1, 1.25:1, 1.5:1, 1.75:1, dan 2:1 (dalam mol). Temperatur pembakaran (atau desulfurisasi) berkisar antara 300-500 °C; waktu reaksi adalah 720 detik dan laju alir udara ditetapkan pada 1,2 L/menit. Hasil penelitian menunjukkan bahwa cangkang kerang hijau dapat ditambahkan dalam pembakaran briket batubara atau biobriket sebagai desulfurizer. Proses desulfurisasi menggunakan desulfurizer tersebut memperlihatkan reaksi order pertama dan efisiensi penyerapan SO2 rata-rata tertinggi adalah 84,5%.

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Section: Use Of Green Mussel Shell As a Desulfurizer In The Blendingsupporting

confidence: 55%

Use of Green Mussel Shell as a Desulfurizer in the Blending of Low Rank Coal-Biomass Briquette Combustion

Mahidin¹,

Gani²,

Hani³

et al. 2016

MST

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“…These antibodies have been used extensively in Western blotting, immunohistochemistry, and localization of hERG channels (Cayabyab and Schlichter, 2002;Wang et al, 2004;Chtcheglova et al, 2008); however, they have not been tested for their electrophysiological effects. We evaluated both antibodies at 100 nM against hERG currents in HEK cells.…”

Section: Resultsmentioning

confidence: 99%

BeKm-1, a Peptide Inhibitor of Human ether-a-go-go-Related Gene Potassium Currents, Prolongs QTc Intervals in Isolated Rabbit Heart

Fang²,

Gao³

et al. 2010

J Pharmacol Exp Ther

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Drug-induced cardiac arrhythmia, specifically Torsades de pointes, is associated with QT/QTc interval prolongation, thus prolongation of the QT interval is considered as a biomarker for Torsades de pointes risk (N Engl J Med 350:1013-1022, 2004). Specific inhibition of human ether-a-go-go-related gene (hERG) potassium channels has been recognized as the main mechanism for QT prolongation (Cardiovasc Res 58:32-45, 2003). This mechanism has been demonstrated for a variety of smallmolecule agents, which access the inner pore of the hERG channel preferentially from inside the cell. Peptide inhibitors of hERG, such as BeKm-1, interact with the extracellular amino acid residues close to the external pore region of the channel. In this study, the isolated rabbit heart was used to assess whether BeKm-1 could induce QTc prolongation like dofetilide and N- [4-[[1-[2-(6-methyl-2-pyridinyl) ethyl]-4-piperidinyl]carbonyl]phenyl]methanesulfonamide (E-4031). Five hearts were perfused with 10 and 100 nM BeKm-1 sequentially. ECG parameters and left ventricular contractility were measured with spontaneously beating hearts. Both concentrations of BeKm-1 prolonged QTc intervals significantly and concentration-dependently (4.7 and 16.3% at 10 and 100 nM, respectively). When evaluated for their inhibitory effect in a hERG functional assay, BeKm-1, dofetilide, and E-4031 caused QTc prolongation at concentrations that caused significant hERG channel inhibition. Lastly, two polyclonal anti-hERG antibodies were also assessed in the hERG channel assay and found to be devoid of any inhibitory effect. These results indicated that the isolated rabbit heart assay can be used to measure QTc changes caused by specific hERG inhibition by peptides that specifically block the external pore region of the channel.

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“…Inflammatory cytokines including TNF-α, interferon-γ, interleukin-1 and interleukin-6 induce superoxide production from vascular smooth muscle cells, endothelial cells [29][30][31] and HEK293 cells [32,33]. TNF-α-inducedoxidative stress in the heart may be mediated by NADPH oxidase, NO synthase and xanthine oxidase enzyme systems, and it contributes to myocardial contractile failure [34].…”

Section: Discussionmentioning

confidence: 99%

Differential upregulation of Nox homologues of NADPH oxidase by tumor necrosis factor‐α in human aortic smooth muscle and embryonic kidney cells

Moe

Aulia

Jiang

et al. 2006

J Cellular Molecular Medi

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Oxidative stress induced by superoxide (O 2¯⋅ ) and other reactive oxygen species (ROS) has critical roles in the pathogenesis of cardiovascular disease [1]. Potential enzymatic sources of ROS in vasculature include the mitochondrial respiration chain, lipoxygenase and cyclooxygenase, xanthine oxidase, NADPH oxidase, nitric oxide (NO) synthase and cytochrome P450 enzymes. Although our understanding of the mechanisms for superoxide production in vascular cells is incomplete, increasing evidence suggests that NADPH oxidase is a AbstractNADPH oxidases are important sources of vascular superoxide, which has been linked to the pathogenesis of atherosclerosis. Previously we demonstrated that the Nox4 subunit of NADPH oxidase is a critical catalytic component for superoxide production in quiescent vascular smooth muscle cells. In this study we sought to determine the role of Nox4 in superoxide production in human aortic smooth muscle cells (AoSMC) and embryonic kidney (HEK293) cells under proinflammatory conditions. Incubation with tumor necrosis factor-α (TNF-α, 10 ng/ml) for 12h increased superoxide production in both cell types, whereas angiotensin II, platelet-derived growth factor or interleukin-1β had little effects. Superoxide production was completely abolished by the NADPH oxidase inhibitors diphenyline iodonium and apocynin, but not by inhibitors of xanthine oxidase, nitric oxide synthase or mitochondrial electron transport. TNF-α upregulated the expression of Nox4 in AoSMC at both message and protein levels, while Nox1 and Nox2 were unchanged. In contrast, upregulation of Nox2 appeared to mediate the enhanced superoxide production by TNF-α in HEK293 cells. We suggest that Nox4 may be involved in increased superoxide generation in vascular smooth muscle cells under proinflammatory conditions.

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Impairment of HERG K+ Channel Function by Tumor Necrosis Factor-α

Cited by 136 publications

References 25 publications

Use of Green Mussel Shell as a Desulfurizer in the Blending of Low Rank Coal-Biomass Briquette Combustion

Use of Green Mussel Shell as a Desulfurizer in the Blending of Low Rank Coal-Biomass Briquette Combustion

BeKm-1, a Peptide Inhibitor of Human ether-a-go-go-Related Gene Potassium Currents, Prolongs QTc Intervals in Isolated Rabbit Heart

Differential upregulation of Nox homologues of NADPH oxidase by tumor necrosis factor‐α in human aortic smooth muscle and embryonic kidney cells

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