Effects of Ca2+channel blockers on store-operated Ca2+channel currents of Kupffer cells after hepatic ischemia/reperfusion injury in rats

Jiang, Nan; Zhang, Zongming; Liu, Liang; Zhang, Chi; Zhang, Yanlu; Zhang, Zi-Chao

doi:10.3748/wjg.v12.i29.4694

Cited by 83 publications

(51 citation statements)

References 31 publications

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“…The results suggest that carvacrol did not cause Ca 2+ influx via stored-operated Ca 2+ entry because carvacrol-induced Ca 2+ entry was not inhibited by three store-operated Ca 2+ entry blockers nifedipine, econazole and SK&F96365. These compounds have been widely applied as blockers of store-operated Ca 2+ entry in Kupffer cells (Ishikawa et al, 2003), T lymphocytes (Jiang et al, 2006) and glioblastoma cells (Hartmann and Verkhratsky, 1998). In the glioblastoma cells (DBTRG-05MG) used in this study, transient receptor potential melastatin 8 ion channels (TRPM8) was suggested to mediate the Ca 2+ entry induced by menthol (Wondergem et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Carvacrol-induced [Ca2+]i rise and apoptosis in human glioblastoma cells

Liang

2012

Life Sciences

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Section: Discussionmentioning

confidence: 99%

Carvacrol-induced [Ca2+]i rise and apoptosis in human glioblastoma cells

Liang

2012

Life Sciences

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“…The data suggest that thymol-induced Ca 2+ entry was inhibited with the three store-operated Ca 2+ entry blockers nifedipine, econazole and SK&F96365. Previous reports have suggested that these chemicals have been used as blockers of store-operated Ca 2+ entry in different cell models [30][31][32] . Because activation of phospholipase C produces inositol 1,4,5-trisphosphate and diacylglycerol, which activates protein kinase C, the effect of modulation of protein kinase C activity on thymolinduced [Ca 2+ ] i rise was examined.…”

Section: Discussionmentioning

confidence: 99%

Effect of Thymol on Ca2+ Homeostasis and Viability in MG63 Human Osteosarcoma Cells

Chang¹,

Hsu²,

Chou

et al. 2011

Pharmacology

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Aims: The effect of the natural product thymol on cytosolic Ca²⁺ concentrations ([Ca²⁺]_i) and viability in MG63 human osteosarcoma cells was examined. Methods: The Ca²⁺-sensitive fluorescent dye fura-2 was applied to measure [Ca²⁺]_i. Results: Thymol at concentrations of 200–1,000 µmol/l induced a [Ca²⁺]_i rise in a concentration-dependent fashion. The response was decreased partially by removal of extracellular Ca²⁺. Thymol-induced Ca²⁺ entry was inhibited by nifedipine, econazole, SK&F96365 and protein kinase C modulators. When extracellular Ca²⁺ was removed, incubation with the endoplasmic reticulum Ca²⁺ pump inhibitor thapsigargin or 2,5-di-tert-butylhydroquinone (BHQ) inhibited the thymol-induced [Ca²⁺]_i rise. Incubation with thymol also inhibited the thapsigargin or BHQ-induced [Ca²⁺]_i rise. Inhibition of phospholipase C with U73122 abolished the thymol-induced [Ca²⁺]_i rise. At concentrations of 100–600 µmol/l, thymol killed cells in a concentration-dependent manner. This cytotoxic effect was not changed by chelating cytosolic Ca²⁺ with 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid/AM. Annexin V/propidium iodide staining data suggest that thymol (200 and 400 µmol/l) induced apoptosis in a concentration-dependent manner. Thymol (200 and 400 µmol/l) also increased levels of reactive oxygen species. Conclusions: In MG63 cells, thymol induced a [Ca²⁺]_i rise by inducing phospholipase C-dependent Ca²⁺ release from the endoplasmic reticulum and Ca²⁺ entry via protein kinase C-sensitive store-operated Ca²⁺ channels. Thymol induced cell death that may involve apoptosis via mitochondrial pathways.

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“…The carvedilol-induced Ca 2þ influx seems to be mediated by a PKC -regulated Ca 2þ entry pathway that does not appear to be store-operated Ca 2þ channels or L-type Ca 2þ channels because the [Ca 2þ ] i rise was not inhibited by four blockers of storeoperated Ca 2þ entry: La 3þ , econazole, SKF96365, and nifedipine. [29][30][31][32][33] How carvedilol induced Ca 2þ influx is unclear. Evidence has shown that carvedilol appears to have a non-specific effect on membranes in phagocytes.…”

Section: Discussionmentioning

confidence: 99%

Carvedilol-induced elevation in cytosolic free Ca2+ level and apoptosis in SIRC corneal epithelial cells

Shieh

Lee

et al. 2009

Hum Exp Toxicol

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The effect of the cardiovascular drug carvedilol on cytosolic free Ca2+ concentrations ([Ca 2+]i) and viability was examined in Statens Seruminstitut rabbit cornea (SIRC) corneal epithelial cells. [Ca2+]i and cell viability were measured using the fluorescent dyes fura-2 and 4-[3-[4-lodophenyl]-2-4(4-nitrophenyl)-2H-5-tetrazolio-1,3-benzene disulfonate] (WST-1), respectively. Carvedilol at concentrations between 1 and 30 μM increased [Ca 2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partly by removing extracellular Ca2+. Carvedilol induced Mn2+ quench of fura-2 fluorescence implicating Ca2+ influx. The Ca2+ influx was inhibited by suppression of protein kinase C activity. In Ca2+-free medium, after pretreatment with 1 μM thapsigargin (an endoplasmic reticulum Ca 2+ pump inhibitor), carvedilol-induced [Ca2+]i rise was reduced; and conversely, carvedilol pretreatment inhibited a major part of thapsigargin-induced [Ca 2+]i rise. Addition of the phospholipase C inhibitor 1-[6-[[17 beta-3-methoxyestra-1,3,5(10)-trien-17-yl]amino] hexyl]-1H-pyrrole-2,5-dione (U73122; 2 μM) did not change carvedilol-induced [Ca2+]i rise. At concentrations between 5 and 70 μM, carvedilol killed cells in a concentration-dependent manner. The cytotoxic effect of 20 μM carvedilol was not reversed by prechelating cytosolic Ca2+ with BAPTA/AM. Apoptosis was induced by 5—70 μM carvedilol. Collectively, in SIRC corneal epithelial cells, carvedilol-induced [Ca2+]i rises by causing Ca2+ release from the endoplasmic reticulum in a phospholipase C-independent manner, and Ca 2+ influx via protein kinase C-regulated Ca2+ channels. Carvedilol-caused cytotoxicity was mediated by Ca2+-independent apoptosis in a concentration-dependent manner.

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Effects of Ca²⁺channel blockers on store-operated Ca²⁺channel currents of Kupffer cells after hepatic ischemia/reperfusion injury in rats

Cited by 83 publications

References 31 publications

Carvacrol-induced [Ca2+]i rise and apoptosis in human glioblastoma cells

Carvacrol-induced [Ca2+]i rise and apoptosis in human glioblastoma cells

Effect of Thymol on Ca<sup>2+</sup> Homeostasis and Viability in MG63 Human Osteosarcoma Cells

Carvedilol-induced elevation in cytosolic free Ca2+ level and apoptosis in SIRC corneal epithelial cells

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