Capacitative Ca2+ entries and mRNA expression for TRPC1 and TRPC5 channels in human epidermoid carcinoma A431 cells

被引:12
|
作者
Yoshida, J [1 ]
Ishibashi, T
Imaizumi, N
Takegami, T
Nishio, M
机构
[1] Kanazawa Med Univ, Dept Pharmacol, Uchinada, Ishikawa 9200293, Japan
[2] Kanazawa Med Univ, Dept Internal Med, Div Endocrinol, Uchinada, Ishikawa 9200293, Japan
[3] Kanazawa Med Univ, Med Res Inst, Div Mol Oncol & Virol, Uchinada, Ishikawa 9200293, Japan
关键词
TRPC1; TRPC5; capacitative Ca2+ entry; human epidermoid carcinoma A431 cell; thapsigargin; uridine 5 '-triphosphate;
D O I
10.1016/j.ejphar.2005.01.029
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
In human epidermoid carcinoma A431 cells, capacitative Ca2+ entries in response to intracellular Ca2+ store depletion with thapsigargin, an endoplasmic reticulum Ca2+-ATPase inhibitor, and uridine 5-triphosphate, a phospholipase C-linked agonist, were inhibited by trivalent cations such as Gd3+ and La3+, and by the store-operated Ca2+ channel inhibitor, 2-aminoethoxydiphenyl borate. Of the seven types of canonical transient receptor potential (TRPC) channels as molecular candidates for store-operated Ca2+ channels, mRNAs for TRPC1 and TRPC5 were detected in the cells with the reverse transcription-polymerase chain reaction. Western blotting confirmed the protein expressions of TRPC1 and TRPC5 in A431 cells. The present results suggest that TRPC1 and/or TRPC5 channels serve as store-operated Ca2+ channels in A431 cells, and may function as regulators for intracellular Ca2+ signaling. (c) 2005 Elsevier B.V. All rights reserved.
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页码:217 / 222
页数:6
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