Response to ADP-ribose by activation of TRPM2 in the CRI-G1 insulinoma cell line

被引:78
作者
Inamura, K [1 ]
Sano, Y [1 ]
Mochizuki, S [1 ]
Yokoi, H [1 ]
Miyake, A [1 ]
Nozawa, K [1 ]
Kitada, C [1 ]
Matsushime, H [1 ]
Furuichi, K [1 ]
机构
[1] Yamanouchi Pharmaceut Co Ltd, Inst Drug Discovery Res, Mol Med Labs, Tsukuba, Ibaraki 3058585, Japan
关键词
ADP-ribose; beta-NAD; TRPM2; CRI-G1; cell; calcium;
D O I
10.1007/s00232-002-1057-x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The response to intracellular ADP-ribose in the rat CRI-G1 insulinoma cell line was studied using a patch-clamp method. Dialysis of ADP-ribose into cells induced a response in a dose-dependent manner. The reversal potentials in various solutions showed that the ADP-ribose-gated channel was a Ca2+-permeable nonselective cation channel. In inside-out recordings, ADP-ribose and beta-NAD induced responses in the same patch. The single-channel current-voltage relationships for ADP-ribose- and beta-NAD-induced responses were almost identical, indicating that ADP-ribose and beta-NAD activated the same channel. The physiological properties of the ADP-ribose-gated channel are similar to those we reported previously for the cloned transient receptor potential channel TRPM2. Moreover, RT-PCR analysis showed that TRPM2 was abundantly expressed in CRI-G1 cells, suggesting that the ADPribose-gated channel represents the native TRPM2 channel in CRI-G1 cells. These results suggest that ADP-ribose can be an endogenous modulator of Ca2+ influx through the TRPM2 channel into CRI-G1 cells.
引用
收藏
页码:201 / 207
页数:7
相关论文
共 40 条
[1]   CA2+ AND PANCREATIC B-CELL FUNCTION [J].
BERGGREN, PO ;
LARSSON, O .
BIOCHEMICAL SOCIETY TRANSACTIONS, 1994, 22 (01) :12-18
[2]   INOSITOL 1,4,5-TRISPHOSPHATE MOBILIZES INTRACELLULAR CA-2+ FROM PERMEABILIZED INSULIN-SECRETING CELLS [J].
BIDEN, TJ ;
PRENTKI, M ;
IRVINE, RF ;
BERRIDGE, MJ ;
WOLLHEIM, CB .
BIOCHEMICAL JOURNAL, 1984, 223 (02) :467-473
[3]  
Duncan LM, 1998, CANCER RES, V58, P1515
[4]  
EFENDIC S, 1991, J INTERN MED, V229, P9
[5]   IMPROVED PATCH-CLAMP TECHNIQUES FOR HIGH-RESOLUTION CURRENT RECORDING FROM CELLS AND CELL-FREE MEMBRANE PATCHES [J].
HAMILL, OP ;
MARTY, A ;
NEHER, E ;
SAKMANN, B ;
SIGWORTH, FJ .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1981, 391 (02) :85-100
[6]   LTRPC2 Ca2+-permeable channel activated by changes in redox status confers susceptibility to cell death [J].
Hara, Y ;
Wakamori, M ;
Ishii, M ;
Maeno, E ;
Nishida, M ;
Yoshida, T ;
Yamada, H ;
Shimizu, S ;
Mori, E ;
Kudoh, J ;
Shimizu, N ;
Kurose, H ;
Okada, Y ;
Imoto, K ;
Mori, Y .
MOLECULAR CELL, 2002, 9 (01) :163-173
[7]   From worm to man: three subfamilies of TRP channels [J].
Harteneck, C ;
Plant, TD ;
Schultz, G .
TRENDS IN NEUROSCIENCES, 2000, 23 (04) :159-166
[8]   Hydrogen peroxide induces intracellular calcium overload by activation of a non-selective cation channel in an insulin-secreting cell line [J].
Herson, PS ;
Lee, K ;
Pinnock, RD ;
Hughes, J ;
Ashford, MLJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (02) :833-841
[9]   Characterization of a nicotinamide-adenine dinucleotide-dependent cation channel in the CRI-G1 rat insulinoma cell line [J].
Herson, PS ;
Dulock, KA ;
Ashford, MLJ .
JOURNAL OF PHYSIOLOGY-LONDON, 1997, 505 (01) :65-76
[10]   Activation of a novel non-selective cation channel by alloxan and H2O2 in the rat insulin-secreting cell line CRI-G1 [J].
Herson, PS ;
Ashford, MLJ .
JOURNAL OF PHYSIOLOGY-LONDON, 1997, 501 (01) :59-66