Store-operated calcium entry promotes shape change in pulmonary endothelial cells expressing Trp1
Store-operated calcium entry promotes shape change in pulmonary endothelial cells expressing Trp1
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DOI：
10.1152/ajplung.1998.275.3.l574
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发表时间：
1998-09-01
影响因子：
4.9
通讯作者：
Stevens, T
中科院分区：
文献类型：
--
作者：
Moore, TM;Brough, GH;Stevens, T
已知Ca 2+进入的激活可产生内皮细胞形状改变，导致血管内皮细胞中的渗透性增加、白细胞迁移和血管生成的启动。Ca 2+进入调节细胞形状的模式尚不清楚。我们假设钙池操纵的钙通道（SOC）的激活足以促进这些过程所需的细胞形状变化。大鼠肺动脉内皮细胞中的SOC活化增加了细胞内游离Ca 2+，这依赖于在-80 mV下具有5.45 +/- 0.90 pA/pF的净向内分量的膜电流。内皮细胞形状的变化伴随SOC激活，并依赖于Ca 2+进入诱导的外周（皮层）丝状肌动蛋白（F-肌动蛋白）的重构。由于肺内皮SOC的身份是未知的，但哺乳动物同源的果蝇瞬时受体电位（trp）基因已被提出形成Ca 2+进入通道的非兴奋细胞，我们进行RT-PCR使用Trp寡核苷酸引物在大鼠和人肺动脉内皮细胞。发现这两种细胞类型表达Trp 1，但既不表达Trp 3也不表达Trp 6。我们的研究表明：1）通过SOC进入肺内皮细胞的Ca 2+导致细胞形状改变，这依赖于微丝骨架的位点特异性重排; 2）Trp 1可能是肺内皮SOC的组成部分。
Activation of Ca2+ entry is known to produce endothelial cell shape change, leading to increased permeability, leukocyte migration, and initiation of angiogenesis in conduit-vessel endothelial cells. The mode of Ca2+ entry regulating cell shape is unknown. We hypothesized that activation of store-operated Ca2+ channels (SOCs) is sufficient to promote cell shape change necessary for these processes. SOC activation in rat pulmonary arterial endothelial cells increased free cytosolic Ca2+ that was dependent on a membrane current having a net inward component of 5.45 +/- 0.90 pA/pF at -80 mV. Changes in endothelial cell shape accompanied SOC activation and were dependent on Ca2+ entry-induced reconfiguration of peripheral (cortical) filamentous actin (F-actin). Because the identity of pulmonary endothelial SOCs is unknown, but mammalian homologues of the Drosophila melanogaster transient receptor potential (trp) gene have been proposed to form Ca2+ entry channels in nonexcitable cells, we performed RT-PCR using Trp oligonucleotide primers in both rat and human pulmonary arterial endothelial cells. Both cell types were found to express Trp1, but neither expressed Trp3 nor Trp6. Our study indicates that 1) Ca2+ entry in pulmonary endothelial cells through SOCs produces cell shape change that is dependent on site-specific rearrangement of the microfilamentous cytoskeleton and 2) Trp1 may be a component of pulmonary endothelial SOCs.