Sun B, Kambayashi J
Vascular Biology, Maryland Research Laboratories, Otsuka America Pharmaceutical, Inc., Rockville, MD 20878, USA.
J Biomed Sci. 2000 Jan-Feb;7(1):35-41. doi: 10.1007/BF02255916.
Ca(2+) influx is an important event associated with platelet activation and regulated by the content of intracellular Ca(2+). Previous studies have suggested two different Ca(2+) pools and two Ca(2+) influx pathways exist in platelets. In the present study, we have investigated the regulation of thrombin- and thapsigargin-induced Ca(2+) entry into human platelets, using fluorescent indicators to monitor Ca(2+) mobilization and membrane potential. It was found that depletion of thapsigargin-sensitive Ca(2+) stores was coupled to Ca(2+) influx through a Ca(2+)-selective pathway. Additional release of Ca(2+) from the thapsigargin-insensitive pool by thrombin caused the opening of a nonselective cation channel.
钙离子内流是与血小板活化相关的重要事件，并受细胞内钙离子含量调控。先前的研究表明血小板中存在两种不同的钙离子池和两条钙离子内流途径。在本研究中，我们使用荧光指示剂监测钙离子动员和膜电位，研究了凝血酶和毒胡萝卜素诱导的钙离子进入人血小板的调控机制。结果发现，毒胡萝卜素敏感的钙离子储存耗尽与通过钙离子选择性途径的钙离子内流相关。凝血酶从毒胡萝卜素不敏感池中额外释放钙离子导致非选择性阳离子通道开放。
