Ca2+ signal is involved in endothelin-1-induced internalization of endothelin type A receptor expressed in Chinese hamster ovary cells
Ca2+ signal is involved in endothelin-1-induced internalization of endothelin type A receptor expressed in Chinese hamster ovary cells
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Ca2信号参与内皮素1诱导的中国仓鼠卵巢细胞表达的内皮素A型受体的内化
DOI：
10.1016/j.jphs.2019.03.008
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发表时间：
2019
影响因子：
3.5
通讯作者：
Miwa Soichi
中科院分区：
文献类型：
--
作者：
Horinouchi Takahiro;Karki Sarita;Terada Koji;Mazaki Yuichi;Miwa Soichi
A 型内皮素受体 (ETAR) 在激动剂刺激下被内化；然而，其机制仍存在争议。在本研究中，我们表征了中国仓鼠卵巢细胞中表达的内皮素-1 (ET-1) 诱导的 ETAR 内化。 ET-1 引起 ETAR 内化并增加细胞内 Ca2+ 浓度。 ET-1 诱导的 ETAR 内化被细胞内和细胞外 Ca2+ 水平的降低完全抑制，并被蛋白激酶 C (PKC) 和细胞外信号调节激酶 1/2 (ERK1/2) 的抑制剂部分抑制，这两者都是 ETAR 信号传导的下游分子。这些结果表明 Ca2+ 动员、PKC 和 ERK1/2 参与 ET-1 诱导的 ETAR 内化。
Endothelin type A receptor (ETAR) is internalized upon agonist stimulation; however, the mechanism thereof remains controversial. In this study, we characterized the endothelin-1 (ET-1)-induced internalization of ETAR expressed in Chinese hamster ovary cells. ET-1 elicited ETAR internalization and increase in intracellular Ca2+concentration. ET-1-induced ETAR internalization was completely inhibited by a reduction in intracellular and extracellular Ca2+levels and partially suppressed by inhibitors of protein kinase C (PKC) and extracellular signal-regulated kinases 1/2 (ERK1/2), both of which are downstream molecules in ETAR signaling. These results suggest that Ca2+mobilization, PKC, and ERK1/2 are involved in ET-1-induced ETAR internalization.