Overexpression of G Protein-Coupled Receptor Kinase 2 Inhibits Neuronal Electrophysiological Activity in SH-SY5Y Cells via Blocking Na Channels; A Laboratory Study
Overexpression of G Protein-Coupled Receptor Kinase 2 Inhibits Neuronal Electrophysiological Activity in SH-SY5Y Cells via Blocking Na Channels; A Laboratory Study
复制标题
G 蛋白偶联受体激酶 2 的过表达通过阻断 Na 通道抑制 SH-SY5Y 细胞中的神经元电生理活动Íο 一项实验室研究
DOI：
10.23812/j.biol.regul.homeost.agents.20223604.126
复制
发表时间：
2022
期刊：
影响因子：
--
通讯作者：
王埮
中科院分区：
文献类型：
--
作者：
马媛媛;许叶;张填;陈志斌;王埮
背景：G蛋白偶联受体激酶2(GRK2)参与G蛋白偶联受体(GPCRs)信号通路和非受体信号通路，是与神经系统疾病发生密切相关的非受体信号通路或既是受体信号又是非受体信号通路。但GRK2在电生理活动中的调控机制尚不清楚。方法：本研究将GRK2 shRNA或GRK2过表达载体分别导入人神经母细胞瘤细胞SH-SY5Y。Western印迹法检测转染效率，膜片钳技术检测GRK2过表达或敲除后SH-SY5Y细胞电生理活性的变化。此外，膜片钳技术显示GRK2过表达显著降低了SH-SY5Y细胞的动作电位放电频率和Na+电流，从而抑制了神经元的兴奋性(p0.05)。结论：GRK2过表达可能通过阻断Na通道而抑制SH-SY5Y细胞的电生理活动。
Background: G protein-coupled receptor kinase 2 (GRK2) is involved in G protein-coupled receptor (GPCRs) pathway and nonreceptor signaling pathway, which is only the non-receptor signaling pathway or both the receptor and non-receptor signaling.pathway closely related to the occurrence of neurological diseases. However, the regulatory mechanism of GRK2 in electrophysiological activity is still unclear..Methods: In this study, GRK2 shRNA plasmid or GRK2 overexpression plasmid was transfected into human neuroblastoma cells.SH-SY5Y. Transfection efficiency was detected using western blot and patch-clamp techniques were used to measure changes in.electrophysiological activity in SH-SY5Y cells after overexpression or knockdown of GRK2..Results: Western blot results showed successful transfection. Additionally, the measurement by patch-clamp technique demonstrated that GRK2 overexpression significantly decreased both action potential firing frequency and Na+ current, which inhibited.neuronal excitability in SH-SY5Y cells (p 0.05)..Conclusions: GRK2 overexpression may suppress the electrophysiological activity of SH-SY5Y cells by blocking the Na channel.