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首页> 外文期刊>Neurochemical Research >Bcl-2 Modulates Endoplasmic Reticulum and Mitochondrial Calcium Stores in PC12 Cells
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Bcl-2 Modulates Endoplasmic Reticulum and Mitochondrial Calcium Stores in PC12 Cells

机译:Bcl-2调节PC12细胞内质网和线粒体钙存储。

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Endoplasmic reticulum (ER) and mitochondria are intracellular organelles and their interactions are directly involved in different processes such as Ca2+ signaling in cell survival and death mechanisms. Bcl-2 is an anti-apoptotic protein intrinsically related to ER and mitochondria, modulating Ca2+ content in these organelles. We investigated the effects of Bcl-2 overexpression on ER and mitochondrial Ca2+ dynamics in PC12 cells. Bcl-2 overexpressing and control cells were loaded with Fura 2/AM and stimulated with different drugs. Results showed that in Bcl-2 cells, ACh induced a lower Ca2+ response compared to control. Ca2+ release induced by TG was decreased in Bcl-2 cells, however, it was greater in Caff induced Ca2+ rise. In addition, FCCP induced a higher Ca2+ release in Bcl-2 cells. These results suggest that Bcl-2 overexpression modulate the ER Ca2+ pools differently and the release of ER Ca2+ may increase mitochondrial Ca2+ accumulation. These alterations of intracellular Ca2+ stores are important mechanisms for the control of Ca2+ signaling.
机译:内质网和线粒体是细胞内的细胞器,它们的相互作用直接参与了不同的过程,例如Ca2 +信号传导在细胞存活和死亡机制中的作用。 Bcl-2是一种与内质网和线粒体内在相关的抗凋亡蛋白,调节这些细胞器中的Ca2 + 含量。我们研究了Bcl-2过表达对PC12细胞内质网和线粒体Ca2 + 动态的影响。 Bcl-2过表达和对照细胞加载Fura 2 / AM,并用不同的药物刺激。结果显示,在Bcl-2细胞中,ACh诱导的Ca2 + 响应较对照组低。 TG诱导的Ca2 + 释放在Bcl-2细胞中降低,而在Caff诱导的Ca2 +升高中则更大。此外,FCCP诱导了Bcl-2细胞中较高的Ca2 + 释放。这些结果表明,Bcl-2过表达调节ER Ca2 + 池的方式不同,释放ER Ca2 + 可能增加线粒体Ca2 + 的积累。细胞内Ca2 + 的这些变化是控制Ca2 + 信号传导的重要机制。

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