|
|
|
|
|
|
|
|
|||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | |||||
Journal of Cell Science, Vol 107, Issue 2 451-462, Copyright © 1994 by Company of Biologists
JOURNAL ARTICLES |
VA Barry and TR Cheek
AFRC Laboratory of Molecular Signalling, Department of Zoology, University of Cambridge, UK.
We have investigated the effects of extracellular ATP on Ca2+ signalling, and its relationship to secretion in rat pheochromocytoma (PC12) cells. In single cells, extracellular ATP evoked two very distinct subcellular distributions of intracellular calcium concentration ([Ca2+]i), only one of which could be mimicked by the pyrimidine nucleotide UTP, suggesting the involvement of more than one cell surface receptor in mediating the ATP-induced responses. ATP and UTP were equipotent in activating a receptor leading to inositol phosphate production and the mobilisation of intracellular Ca2+. In some cells (19%) this rise in [Ca2+]i initiated at a discrete site and then propagated across the cell in the form of a Ca2+ wave. In addition to mobilising intracellular Ca2+ through a 'nucleotide' receptor sensitive to ATP and UTP, the results indicate that ATP also activates divalent cation entry through an independent receptor-operated channel. Firstly, ATP-induced entry of Ca2+ or Mn2+ was independent of Ca2+ mobilisation, as prior treatment of cell populations with UTP abolished the ATP-evoked release of intracellular Ca2+ stores, but left the Ca(2+)- and Mn(2+)-entry components uneffected. Secondly, although UTP and ATP were equally effective in generating inositol phosphates, only ATP stimulated divalent cation entry, indicating that ATP-activated influx was independent of phosphoinositide turnover. Thirdly, single cell experiments revealed a subpopulation of cells that responded to ATP with divalent cation entry without mobilising Ca2+ from intracellular stores. Lastly, the dihydropyridine antagonist, nifedipine, reduced the ATP-induced rise in [Ca2+]i by only 24%, suggesting that Ca2+ entry was largely independent of L-type voltage-operated Ca2+ channels. The Ca2+ signals could also be distinguished at a functional level. Activation of ATP-induced divalent cation influx was absolutely required to evoke transmitter release, because ATP triggered secretion of [3H]dopamine only in the presence of external Ca2+, and UTP was unable to promote secretion, irrespective of the extracellular [Ca2+]. The results suggest that the same extracellular stimulus can deliver different Ca2+ signals into the same cell by activating different Ca2+ signalling pathways, and that these Ca2+ signals can be functionally distinct.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati 
Twitter What's this?
This article has been cited by other articles:
|
|
 |
|
  J. Yue, W. Wei, C. M. C. Lam, Y.-J. Zhao, M. Dong, L.-R. Zhang, L.-H. Zhang, and H.-C. Lee CD38/cADPR/Ca2+ Pathway Promotes Cell Proliferation and Delays Nerve Growth Factor-induced Differentiation in PC12 Cells J. Biol. Chem., October 23, 2009; 284(43): 29335 - 29342. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Rajebhosale, S. Greenwood, J. Vidugiriene, A. Jeromin, and S. Hilfiker Phosphatidylinositol 4-OH Kinase Is a Downstream Target of Neuronal Calcium Sensor-1 in Enhancing Exocytosis in Neuroendocrine Cells J. Biol. Chem., February 14, 2003; 278(8): 6075 - 6084. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B.-C. Suh, H. Lee, D.-J. Jun, J.-S. Chun, J.-H. Lee, and K.-T. Kim Inhibition of H2 Histamine Receptor-Mediated Cation Channel Opening by Protein Kinase C in Human Promyelocytic Cells J. Immunol., August 1, 2001; 167(3): 1663 - 1671. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B.-C. Suh, J.-S. Kim, U. Namgung, H. Ha, and K.-T. Kim P2X7 Nucleotide Receptor Mediation of Membrane Pore Formation and Superoxide Generation in Human Promyelocytes and Neutrophils J. Immunol., June 1, 2001; 166(11): 6754 - 6763. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E.-M. Hur, T.-J. Park, and K.-T. Kim Coupling of L-type voltage-sensitive calcium channels to P2X2 purinoceptors in PC-12 cells Am J Physiol Cell Physiol, May 1, 2001; 280(5): C1121 - C1129. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Chen, D. Maruyama, M. Sugiyama, T. Sakai, C. Mogi, M. Kato, R. Kurotani, N. Shirasawa, A. Takaki, U. Renner, et al. Cytological Characterization of a Pituitary Folliculo-Stellate-Like Cell Line, Tpit/F1, with Special Reference to Adenosine Triphosphate-Mediated Neuronal Nitric Oxide Synthase Expression and Nitric Oxide Secretion Endocrinology, October 1, 2000; 141(10): 3603 - 3610. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. P. Soltoff Related Adhesion Focal Tyrosine Kinase and the Epidermal Growth Factor Receptor Mediate the Stimulation of Mitogen-activated Protein Kinase by the G-protein-coupled P2Y2 Receptor. PHORBOL ESTER OR [Ca2+]i ELEVATION CAN SUBSTITUTE FOR RECEPTOR ACTIVATION J. Biol. Chem., September 4, 1998; 273(36): 23110 - 23117. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Ralevic and G. Burnstock Receptors for Purines and Pyrimidines Pharmacol. Rev., September 1, 1998; 50(3): 413 - 492. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. D. Swanson, C. Reigh, and G. E. Landreth ATP-stimulated Activation of the Mitogen-activated Protein Kinases through Ionotrophic P2X2 Purinoreceptors in PC12 Cells. DIFFERENCE IN PURINORECEPTOR SENSITIVITY IN TWO PC12 CELL LINES J. Biol. Chem., August 7, 1998; 273(32): 19965 - 19971. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. P. Soltoff, H. Avraham, S. Avraham, and L. C. Cantley Activation of P2Y2 Receptors by UTP and ATP Stimulates Mitogen-activated Kinase Activity through a Pathway That Involves Related Adhesion Focal Tyrosine Kinase and Protein Kinase C J. Biol. Chem., January 30, 1998; 273(5): 2653 - 2660. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Jackson, I. Blader, L. Hammonds-Odie, C. Burga, F Cooke, P. Hawkins, A. Wolf, K. Heldman, and A. Theibert Initiation and maintenance of NGF-stimulated neurite outgrowth requires activation of a phosphoinositide 3-kinase J. Cell Sci., January 2, 1996; 109(2): 289 - 300. [Abstract] [PDF]
|
|
