Capacitative calcium entry supports calcium oscillations in human embryonic kidney cells

被引:98
作者
Bird, GS [1 ]
Putney, JW [1 ]
机构
[1] NIEHS, Lab Signal Transduct, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA
来源
JOURNAL OF PHYSIOLOGY-LONDON | 2005年 / 562卷 / 03期
关键词
D O I
10.1113/jphysiol.2004.077289
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Treatment of human epithelial kidney (HEK293) cells with low concentrations of the muscarinic agonist methacholine results in the activation of complex and repetitive cycling of intracellular calcium ([Ca2+](i)), known as [Ca2+](i) oscillations. These oscillations occur with a frequency that depends on the concentration of methacholine, whereas the magnitude of the [Ca2+](i) spikes does not. The oscillations do not persist in the absence of extracellular Ca2+, leading to the conclusion that entry of Ca2+ across the plasma membrane plays a significant role in either their initiation or maintenance. However, treatment of cells with high concentrations of GdCl3, a condition which limits the flux of calcium ions across the plasma membrane in both directions, allows sustained [Ca2+], oscillations to occur. This suggests that the mechanisms that both initiate and regenerate [Ca2+](i) Oscillations are intrinsic to the intracellular milieu and do not require entry of extracellular Ca2+. This would additionally suggest that, under normal conditions, the role of calcium entry is to sustain [Ca2+](i) oscillations. By utilizing relatively specific pharmacological manoeuvres we provide evidence that the Ca2+ entry that supports Ca2+ oscillations occurs through the store-operated or capacitative calcium entry pathway. However, by artificial introduction of a non-store-operated pathway into the cells (TRPC3 channels), we find that other Ca2+ entry mechanisms can influence oscillation frequency in addition to the store-operated channels.
引用
收藏
页码:697 / 706
页数:10
相关论文
共 29 条
  • [1] Berridge Michael J., 1992, Advances in Second Messenger and Phosphoprotein Research, V26, P211
  • [2] INOSITOL TRISPHOSPHATE AND CALCIUM SIGNALING
    BERRIDGE, MJ
    [J]. NATURE, 1993, 361 (6410) : 315 - 325
  • [3] CAPACITATIVE CALCIUM-ENTRY
    BERRIDGE, MJ
    [J]. BIOCHEMICAL JOURNAL, 1995, 312 : 1 - 11
  • [4] Elementary and global aspects of calcium signalling
    Berridge, MJ
    [J]. JOURNAL OF PHYSIOLOGY-LONDON, 1997, 499 (02): : 291 - 306
  • [5] Mechanisms of phospholipase C-regulated calcium entry
    Bird, GS
    Aziz, O
    Lievremont, JP
    Wedel, BJ
    Trebak, M
    Vazquez, G
    Putney, JW
    [J]. CURRENT MOLECULAR MEDICINE, 2004, 4 (03) : 291 - 301
  • [6] Role of the phospholipase C-inositol 1,4,5-trisphosphate pathway in calcium release-activated calcium current and capacitative calcium entry
    Broad, LM
    Braun, FJ
    Lievremont, JP
    Bird, GSJ
    Kurosaki, T
    Putney, JW
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (19) : 15945 - 15952
  • [7] VASOPRESSIN STIMULATION OF CA2+ MOBILIZATION, 2 BIVALENT CATION ENTRY PATHWAYS AND CA2+ EFFLUX IN A7R5 RAT SMOOTH-MUSCLE CELLS
    BYRON, KL
    TAYLOR, CW
    [J]. JOURNAL OF PHYSIOLOGY-LONDON, 1995, 485 (02): : 455 - 468
  • [8] CA-2+ OSCILLATIONS IN NONEXCITABLE CELLS
    FEWTRELL, C
    [J]. ANNUAL REVIEW OF PHYSIOLOGY, 1993, 55 : 427 - 454
  • [9] Relationship between intracellular calcium store depletion and calcium release-activated calcium current in a mast cell line (RBL-1)
    Huang, Y
    Putney, JW
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (31) : 19554 - 19559
  • [10] EVIDENCE FOR 2 PATHWAYS OF RECEPTOR-MEDIATED CA2+ ENTRY IN HEPATOCYTES
    LLOPIS, J
    KASS, GEN
    GAHM, A
    ORRENIUS, S
    [J]. BIOCHEMICAL JOURNAL, 1992, 284 : 243 - 247