Open AccessProtein interacting with C-kinase 1 modulates exocytosis and KATP conductance in pancreatic β cells
Author(s) -
Yunhong Li,
Fan Li,
Bin Bai,
Zhenyong Wu,
Xiaolin Hou,
Ying Shen,
Yin Wang
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.7056
Subject(s) - exocytosis , glutamate receptor , microbiology and biotechnology , biology , biochemistry , receptor , secretion
It has been previously identified that α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptors (AMPARs) are expressed in pancreatic β cells and regulate exocytosis and insulin release. It is known that protein interacting with C‑kinase 1 (PICK1) regulates trafficking and synaptic targeting of AMPARs in the central nervous system. However, it is unknown whether PICK1 regulates glutamate‑induced insulin release in β cells. The present study demonstrated that glutamate‑induced exocytosis was increased in β cells derived from PICK1‑knockout mice. In agreement with this result, adding PICK1 in β cells reduced glutamate‑induced exocytosis, whereas adding EVKI, a peptide that interrupts the interaction between AMPARs and PICK1, increased the exocytosis of β cells with the application of glutamate. Furthermore, the conductance of ATP‑sensitive potassium (KATP) channels was reduced in PICK1‑knockout mice, which was reversed by the overexpression of PICK1. In addition, PICK1 application reduced voltage oscillation induced by the closure of KATP. Taken together, the results indicate that PICK1 regulates glutamate‑induced exocytosis in β cells.