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首页> 外文期刊>Journal of receptor and signal transduction research >Investigation of carvedilol-evoked Ca~(2+) movement and death in human oral cancer cells
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Investigation of carvedilol-evoked Ca~(2+) movement and death in human oral cancer cells

机译：卡维地洛诱发的人口腔癌细胞中Ca〜（2+）运动和死亡的研究

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The effect of carvedilol on cytosolic free Ca~(2+) concentrations ([Ca~(2+)]i) in OC2 human oral cancer cells is unknown. This study examined if carvedilol altered basal [Ca~(2+)]i levels in suspended OC2 cells by using fura-2 as a Ca~(2+)-sensitive fluorescent probe. Carvedilol at concentrations between 10 and 40 μM increased [Ca ~(2+)]i in a concentration-dependent fashion. The Ca~(2+) signal was decreased by 50% by removing extracellular Ca~(2+). Carvedilol-induced Ca~(2+) entry was not affected by the store-operated Ca~(2+) channel blockers nifedipine, econazole, and SK&F96365, but was enhanced by activation or inhibition of protein kinase C. In Ca ~(2+)-free medium, incubation with the endoplasmic reticulum Ca ~(2+) pump inhibitor thapsigargin did not change carvedilol-induced [Ca~(2+)]i rise; conversely, incubation with carvedilol did not reduce thapsigargin-induced Ca~(2+) release. Pretreatment with the mitochondrial uncoupler carbonylcyanide m-chlorophenylhydrazone (CCCP) inhibited carvedilol-induced [Ca~(2+)]i release. Inhibition of phospholipase C with U73122 did not alter carvedilol-induced [Ca~(2+)]i rise. Carvedilol at 5-50 μM induced cell death in a concentration-dependent manner. The death was not reversed when cytosolic Ca~(2+) was chelated with 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid acetoxymethyl ester (BAPTA/AM). Annexin V/propidium iodide staining assay suggests that apoptosis played a role in the death. Collectively, in OC2 cells, carvedilol induced [Ca~(2+)]i rise by causing phospholipase C-independent Ca~(2+) release from mitochondria and non-endoplasmic reticulum stores, and Ca~(2+) influx via protein kinase C-regulated channels. Carvedilol (up to 50 μ?M) induced cell death in a Ca ~(2+)-independent manner that involved apoptosis.
机译：卡维地洛对OC2人口腔癌细胞中胞质游离Ca〜（2+）浓度（[Ca〜（2 +）] i）的影响尚不清楚。这项研究通过使用fura-2作为对Ca〜（2+）敏感的荧光探针检测卡维地洛是否改变了悬浮OC2细胞中的基础[Ca〜（2 +）] i水平。卡维地洛浓度在10到40μM之间，以浓度依赖的方式增加[Ca〜（2 +）] i。通过去除细胞外Ca〜（2 +），Ca〜（2+）信号降低了50％。卡维地洛诱导的Ca〜（2+）进入不受存储操纵的Ca〜（2+）通道阻滞剂硝苯地平，益康唑和SK＆F96365的影响，但通过激活或抑制蛋白激酶C增强。 +）无培养基，与内质网Ca〜（2+）泵抑制剂毒胡萝卜素一起孵育不会改变卡维地洛诱导的[Ca〜（2 +）] i升高;相反，与卡维地洛一起孵育并不能减少毒胡萝卜素诱导的Ca〜（2+）释放。线粒体解偶联剂羰基氰化物间氯苯hydr（CCCP）预处理抑制卡维地洛诱导的[Ca〜（2 +）] i释放。用U73122抑制磷脂酶C不会改变卡维地洛诱导的[Ca〜（2 +）] i升高。 5-50μM的卡维地洛以浓度依赖的方式诱导细胞死亡。当胞质Ca〜（2+）与1,2-双（2-氨基苯氧基）乙烷-N，N，N'，N'-四乙酸乙酰氧基甲基酯（BAPTA / AM）螯合时，死亡没有逆转。 Annexin V /碘化丙啶染色法表明凋亡在死亡中起作用。集体地，在OC2细胞中，卡维地洛通过引起线粒体和非内质网存储区释放磷脂酶C依赖性Ca〜（2+）释放，并通过蛋白质流入Ca〜（2+），从而诱导[Ca〜（2 +）] i升高。激酶C调节的通道。卡维地洛（高达50μM）以不依赖Ca〜（2+）的方式诱导细胞死亡，涉及细胞凋亡。

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