Gende O A
Centro de Investigaciones Cardiovasculares, Universidad Nacional de La Plata, 60 Y 120, La Plata, 1900, Argentina.
Biochem Biophys Res Commun. 2000 Jan 19;267(2):546-50. doi: 10.1006/bbrc.1999.2002.
Ca(2+) release from internal stores as a result of activation of phospholipase C or inhibition of the endoplasmic reticulum pump is accompanied by Ca(2+) influx from the extracellular space. Measurement of intracellular calcium concentration and fluorescence quenching in Fura2-loaded cells showed that platelets preincubated in lithium have significantly higher basal, but lower agonist-stimulated influx of Mn(2+) (acting as a surrogate of Ca(2+) influx), than platelets reloaded with calcium in a normal sodium medium. There is no difference in the basal entry of divalent ion in platelets preincubated in sodium, lithium, or N-methyl glucamine in the absence of calcium. In platelets preincubated in lithium there is a higher basal Mn(2+) entry without further increase upon store depletion by thapsigargin. In contrast, a significant increase in the divalent ion influx was found in sodium or N-methyl glucamine attributable to the opening of channels sensitive to store depletion. In the absence of extracellular calcium, the empty store opens channels and Li(+) did not have additional effect on channels that are already open. The refilling of the stores with Ca(2+) suppresses Mn(2+) entry after sodium or NMG preincubation, but not after lithium preincubation. We propose that lithium induces a calcium influx throughout store-operated channels. This hypothesis may explain the lack of additivity, in cell preincubated in lithium, of basal entry and thapsigargin-triggered entry of calcium.
由于磷脂酶C的激活或内质网泵的抑制导致细胞内钙库释放Ca(2+)，同时伴有细胞外空间Ca(2+)内流。对Fura2负载细胞内钙浓度和荧光猝灭的测量表明，与在正常钠培养基中重新加载钙的血小板相比，预先在锂中孵育的血小板具有显著更高的基础水平，但激动剂刺激的Mn(2+)（作为Ca(2+)内流的替代物）内流较低。在无钙情况下，预先在钠、锂或N-甲基葡糖胺中孵育的血小板中二价离子的基础内流没有差异。在预先在锂中孵育的血小板中，基础Mn(2+)内流较高，在用毒胡萝卜素耗尽钙库后没有进一步增加。相反，在钠或N-甲基葡糖胺中发现二价离子内流显著增加，这归因于对钙库耗尽敏感的通道开放。在没有细胞外钙的情况下，空的钙库打开通道，Li(+)对已经开放的通道没有额外影响。在用Ca(2+)重新填充钙库后，钠或NMG预孵育后Mn(2+)内流受到抑制，但锂预孵育后没有。我们提出锂通过钙库操纵通道诱导钙内流。这一假设可能解释了在锂预孵育的细胞中，基础钙内流和毒胡萝卜素触发的钙内流缺乏相加性的现象。
