Ca2+ store-independent augmentation of [Ca2+]i responses to G-protein coupled receptor activation in recombinantly TRPC5-expressed rat pheochromocytoma (PC12) cells

Ca2+ store-independent augmentation of [Ca2+]i responses to G-protein coupled receptor activation in recombinantly TRPC5-expressed rat pheochromocytoma (PC12) cells
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DOI:
10.1016/j.neulet.2004.01.028
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发表时间:
2004-04
影响因子:
2.5
通讯作者:
T. Ohta;M. Morishita;Y. Mori;S. Ito
T. Ohta;M. Morishita;Y. Mori;S. Ito
中科院分区:
医学4区
文献类型:
--
作者:
T. Ohta;M. Morishita;Y. Mori;S. Ito

文献摘要

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果蝇典型瞬时受体电位(trp)蛋白(TRPC)的哺乳动物同源物被认为具有受体操纵的钙通道(ROCs)或钙库操纵的钙通道(SOCs)的功能。为了确定TRPC 5蛋白在神经细胞中的作用,在大鼠嗜铬细胞瘤细胞(PC 12)中重组表达TRPC 5,并分析细胞内Ca 2+浓度([Ca 2 +]i)和Na+浓度([Na+]i)的变化。TRPC 1和TRPC 3 mRNA在PC 12细胞中内源性表达。TRPC-5表达细胞的静息[Ca ~(2+)] i和[Na ~+] i显著高于对照细胞。缓激肽和5′-三磷酸尿苷引起的TRPC 5-细胞内[Ca ~(2+)] i升高幅度明显大于缓激肽和5′-三磷酸尿苷。TRPC 5的表达没有改变,在存储操作的钙离子内流引起的毒胡萝卜素。TRPC 5-细胞对BK反应的内向电流和[Na+] i增加。这些结果表明,在PC 12细胞中表达的TRPC 5通道作为由G-蛋白/磷脂酶C偶联受体激活的ROCs而不是作为SOC发挥功能。
Mammalian homologues of the Drosophila canonical transient receptor potential (trp) protein (TRPC) have been implicated to function as receptor-operated Ca2+channels (ROCs) or store-operated Ca2+channels (SOCs). To determine the role of TRPC5 protein in neural cells, TRPC5 was recombinantly expressed in rat pheochromocytoma cells (PC12) and changes in intracellular Ca2+concentration ([Ca2+]i) and Na+concentration ([Na+]i) were analyzed. TRPC1 and TRPC3 mRNAs were endogenously expressed in PC12 cells. In TRPC5-expressed cells (TRPC5-cells), the resting [Ca2+]iand [Na+]iwere significantly higher than those in control cells. The [Ca2+]iincreases induced by bradykinin and uridine 5′-triphosphate were significantly larger in TRPC5-cells. TRPC5 expression did not change in store-operated Ca2+entry elicited by thapsigarigin. TRPC5-cells showed larger inward current and increase of [Na+]iin response to BK than control cells. These results suggest that TRPC5 channels expressed in PC12 cells function as ROCs activated by G-protein/phospholipase C coupled receptors, but not as SOCs.