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首页> 外文期刊>Biological & pharmaceutical bulletin >Mitochondria take up Ca ~(2+) in two steps dependently on store-operated Ca ~(2+) entry in mast cells
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Mitochondria take up Ca ~(2+) in two steps dependently on store-operated Ca ~(2+) entry in mast cells

机译：线粒体分两步吸收钙〜（2+），这取决于肥大细胞中存储操作的钙〜（2+）的进入

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The ability of mitochondria to take up Ca ~(2+) has important functional implications for modulation of cellular Ca ~(2+) signaling. Mitochondrial Ca ~(2+) uptake is stimulated by an increase in cytosolic Ca ~(2+) concentration ([Ca ~(2+)] _c). Here, we found that the increase in mitochondrial Ca ~(2+) concentration ([Ca ~(2+)] _m) occurs in two steps in a single antigen-activated mast cell in the presence of extracellular Ca ~(2+) (1.0 mM). The two-step elevation of [Ca ~(2+)] m was also observed after adding thapsigargin, an inhibitor of sarcoplasmic/endoplasmic reticulum Ca ~(2+)-ATPase. The proportion of mitochondria showing the two-step Ca ~(2+) elevation dropped off in direct accord with decrease in extracellular Ca ~(2+) concentration. The second step of the [Ca ~(2+)] m increase was suppressed significantly in the absence of extracellular Ca ~(2+) and in knockdown cells of stromal interaction molecule 1 (STIM1), an essential molecule on endoplasmic reticulum (ER) membrane for store-operated Ca ~(2+)entry, in the presence of extracellular Ca ~(2+) (1.0 mM), while the first elevation was not affected in either case. The results indicate that mitochondria take up cytosolic Ca ~(2+) in two steps; first and second uptakes are derived from the Ca ~(2+) release from ER and the Ca ~(2+) influx through store-operated Ca ~(2+) channels, respectively. Additionally, rotenone and antimycin A, which are inhibitors of mitochondrial electron transport complex I and III, respectively, diminished mitochondrial Ca ~(2+) uptake and significantly suppressed degranulation stimulated with antigen. The mitochondrial Ca ~(2+) uptake may modulate mast cell function by regulating the [Ca ~(2+)] _c.
机译：线粒体吸收Ca〜（2+）的能力对于调节细胞Ca〜（2+）信号传导具有重要的功能意义。线粒体Ca〜（2+）浓度（[Ca〜（2+）] _c）的增加刺激了线粒体Ca〜（2+）的吸收。在这里，我们发现在存在细胞外Ca〜（2+）的情况下，单个抗原激活的肥大细胞中线粒体Ca〜（2+）浓度（[Ca〜（2+）] _m）的增加分两步发生。 （1.0毫米）。在添加thapsigargin（肌浆/内质网Ca〜（2 +）-ATPase的抑制剂）后，也观察到了[Ca〜（2+）] m的两步升高。线粒体比例呈两步上升，Ca〜（2+）下降与细胞外Ca〜（2+）浓度降低直接相关。 [Ca〜（2+）] m增加的第二步在不存在细胞外Ca〜（2+）以及内质网（ER）必需分子间质相互作用分子1（STIM1）的敲低细胞中得到显着抑制在细胞外Ca〜（2+）（1.0 mM）存在的情况下，用于存储操作的Ca〜（2+）入口的膜，而这两种情况下的第一次升高都不受影响。结果表明线粒体分两步吸收胞质Ca〜（2+）。第一次摄取和第二次摄取分别来自于ER释放的Ca〜（2+）和通过存储操作的Ca〜（2+）通道流入的Ca〜（2+）。此外，鱼藤酮和抗霉素A分别是线粒体电子传递复合体I和III的抑制剂，可减少线粒体Ca〜（2+）的吸收并显着抑制抗原刺激下的脱粒。线粒体Ca〜（2+）的摄取可通过调节[Ca〜（2+）] _c来调节肥大细胞功能。

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