Journal
JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
Volume 36, Issue 4, Pages 1155-1160Publisher
BIOLIFE SAS
DOI: 10.23812/j.biol.regul.homeost.agents.20223604.126
Keywords
G protein-coupled receptor kinase 2; electrophysiology; Na plus channels
Funding
- General Project of Na-tional Natural Science Foundation
- Hainan Province Clinical Medical Center
- [81860243]
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This study found that GRK2 suppresses the electrophysiological activity of SH-SY5Y cells by blocking the Na channel, which may have implications for the occurrence of neurological diseases.
Background: G protein-coupled receptor kinase 2 (GRK2) is involved in G protein-coupled receptor (GPCRs) pathway and non -receptor 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 electrophys-iological 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 demon-strated that GRK2 overexpression significantly decreased both action potential firing frequency and Na+ current, which inhibited neuronal excitability in SH-SY5Y cells (p < 0.05). However, knockdown of GRK2 had no significant effect on action potential firing frequency and Na+ current in SH-SY5Y cells (p > 0.05). Conclusions: GRK2 overexpression may suppress the electrophysiological activity of SH-SY5Y cells by blocking the Na channel.
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