Martínez-Zaguilán R, Wesson D E
Department of Physiology, Texas Tech University Health Sciences Center, Lubbock 79430, USA.
Miner Electrolyte Metab. 1996;22(5-6):318-35.
This paper reviews work by our and other laboratories that explores the coupling between glycolysis and endoplasmic reticulum (ER)-Ca-ATPases in regulating Ca2+ homeostasis in several cell types. Changes in intracellular Ca2+ [(Ca2+]in) link interaction between hormones and cell surface receptors with the initiation of specific cellular functions. Thus, changes in [Ca2+]in mediate signal transduction mechanisms that modulate many physiological functions including cell growth, muscle cell contractility, and exocytosis in secretory cells. In most eukaryotic cells, total cellular Ca2+ is in the millimolar range, yet only a fraction (i.e., nanomolar) is free in the cytosol. Cells use both active and 'passive' mechanisms to maintain [Ca2+]in within a narrow range. Active mechanisms include plasma membrane and endoplasmic/sarcoplasmic reticulum (ER/SR)-Ca-ATPases, Ca2+ channels (inositol trisphosphate- and voltage-sensitive), and Na+/Ca2+ exchangers. 'Passive' mechanisms include Ca(2+)-binding proteins (e.g., calsequestrin, calmodulin, calreticulin). The relative contribution of active and 'passive' mechanisms to [Ca2+]in homeostasis in a given cell is not known. Ca2+ might move among several intracellular compartments, including the ER/SR, mitochondria, nucleus, Golgi apparatus, endosomes and lysosomes. The ubiquitous distribution of ER-Ca-ATPases in these intracellular organelles suggests a major role of this pump in Ca2+ homeostasis, but the importance of intracellular compartments to [Ca2+]in homeostasis is not well understood. Glucose has been suggested to have a role in regulating some of these ion transport processes. Thus, the increased cell metabolism that follows glucose stimulation is associated with altered [Ca2+]in homeostasis. The precise mechanisms by which glucose or its metabolites modulate [Ca2+]in homeostasis are unknown but might involve regulation of ER-Ca-ATPases.
本文综述了我们实验室及其他实验室的研究工作，这些研究探讨了糖酵解与内质网（ER）-Ca-ATP酶之间的偶联在调节多种细胞类型中Ca2+稳态方面的作用。细胞内Ca2+（[Ca2+]in）的变化将激素与细胞表面受体之间的相互作用与特定细胞功能的启动联系起来。因此，[Ca2+]in的变化介导了信号转导机制，调节许多生理功能，包括细胞生长、肌肉细胞收缩以及分泌细胞中的胞吐作用。在大多数真核细胞中，细胞内总Ca2+处于毫摩尔范围内，但只有一小部分（即纳摩尔）在细胞质中是游离的。细胞利用主动和“被动”机制将[Ca2+]in维持在狭窄范围内。主动机制包括质膜和内质网/肌浆网（ER/SR）-Ca-ATP酶、Ca2+通道（对肌醇三磷酸和电压敏感）以及Na+/Ca2+交换体。“被动”机制包括Ca(2+)-结合蛋白（如肌浆网钙结合蛋白、钙调蛋白、钙网蛋白）。在给定细胞中，主动和“被动”机制对[Ca2+]in稳态的相对贡献尚不清楚。Ca2+可能在几个细胞内区室之间移动，包括ER/SR、线粒体、细胞核、高尔基体、内体和溶酶体。ER-Ca-ATP酶在这些细胞内细胞器中的普遍分布表明该泵在Ca2+稳态中起主要作用，但细胞内区室对[Ca2+]in稳态的重要性尚未得到充分理解。有人提出葡萄糖在调节其中一些离子转运过程中起作用。因此，葡萄糖刺激后细胞代谢的增加与[Ca2+]in稳态的改变有关。葡萄糖或其代谢产物调节[Ca2+]in稳态的确切机制尚不清楚，但可能涉及对ER-Ca-ATP酶的调节。
