Receptor-operated osteoclast calcium sensing.
Receptor-operated osteoclast calcium sensing.
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DOI：
10.1210/endo.142.5.8125
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发表时间：
2001-05
期刊：
影响因子：
4.8
通讯作者：
B. Bennett;U. Alvarez;K. Hruska
中科院分区：
文献类型：
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作者：
B. Bennett;U. Alvarez;K. Hruska
破骨细胞“感知”升高的细胞外钙，导致细胞骨架变化，这可能与磷脂酶C（PLC）激活和相关的细胞内钙（[Ca（2+）]（i））升高有关。由于PLC与瞬时受体电位通道（trp）相关，我们假设由于这种通道类型引起的受体激活钙内流将被破骨细胞感知[Ca（2+）]激活（e）。我们发现，高[Ca（2+）]（e）诱导了鸡破骨细胞中类似的细胞内Ca（2+）升高，有或没有细胞内Ca（2+）库被TPEN或毒胡萝卜素耗尽，从而定义了钙库不敏感的Ca（2+）内流。PLC拮抗剂U73122可阻断这种钙池不敏感的钙敏感成分。此外，钙通道抑制剂SKF 96365，一种非依赖于储存的色氨酸样通道的阻断剂，在毒胡萝卜素存在下有效抑制钙敏感。因此，钙传感的一个独立的存储组件与连接到PLC的离子通道。由于受体激活的瞬时受体电位（trp）家族阳离子通道以PLC依赖性和非储存依赖性的方式打开，我们认为受体操纵的通道在高细胞外Ca（2+）刺激的破骨细胞中被激活。
Osteoclasts "sense" elevated extracellular calcium, which leads to cytoskeletal changes that may be linked to phospholipase C (PLC) activation and the associated rise in intracellular calcium ([Ca(2+)](i)). Since PLC is linked to transient receptor potential channels (trp), we hypothesized that receptor activated calcium influx due to this channel type would be activated by osteoclasts sensing [Ca(2+)](e). We found that high [Ca(2+)](e) induced similar intracellular Ca(2+) rises in chicken osteoclasts with or without intracellular Ca(2+) store depletion by either TPEN or thapsigargin, thus defining store-insensitive Ca(2+) influx. This store-insensitive calcium sensing component was blocked by the PLC antagonist U73122. Also, the calcium channel inhibitor SKF 96365, a blocker of store-independent trp-like channels, was effective in inhibiting calcium sensing in the presence of thapsigargin. Thus, a store-independent component of calcium sensing was associated with ion channels linked to PLC. Since receptor activated transient receptor potential (trp) family cation channels open in a PLC-dependent and store-independent manner, we suggest that receptor operated channels are activated in osteoclasts stimulated by high extracellular Ca(2+).