P2 Receptor Signalling, Proliferation of Astrocytes, and Expression of Molecules Involved in Cell–Cell Interactions

  1. Derek J. Chadwick Organizer and
  2. Jamie Goode
  1. Joseph T. Neary,
  2. Yuan Kang,
  3. You-Fang Shi,
  4. Minh D. Tran and
  5. Ina B. Wanner

Published Online: 7 OCT 2008

DOI: 10.1002/9780470032244.ch11

Purinergic Signalling in Neuron-Glia Interactions: Novartis Foundation Symposium 276

Purinergic Signalling in Neuron-Glia Interactions: Novartis Foundation Symposium 276

How to Cite

Neary, J. T., Kang, Y., Shi, Y.-F., Tran, M. D. and Wanner, I. B. (2006) P2 Receptor Signalling, Proliferation of Astrocytes, and Expression of Molecules Involved in Cell–Cell Interactions, in Purinergic Signalling in Neuron-Glia Interactions: Novartis Foundation Symposium 276 (eds D. J. Chadwick and J. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470032244.ch11

Author Information

  1. Research Service 151, Veterans Affairs Medical Center, and Departments of Pathology, Biochemistry & Molecular Biology, Neurological Surgery, Neuroscience Program and Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, 1201 NW 16th Street, Miami, FL, 33125, USA

Publication History

  1. Published Online: 7 OCT 2008
  2. Published Print: 21 APR 2006

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470018606

Online ISBN: 9780470032244

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Keywords:

  • glial fibrillary acidic protein (GFAP);
  • P2 receptor and astrocyte proliferation;
  • P2 receptor signalling;
  • fibroblast growth factor (FGF)2 and astrocyte proliferation;
  • purinergic signalling via protein kinase cascades

Summary

Growing evidence indicates that trophic actions of extracellular nucleotides are involved in CNS development, injury and repair. For example, upon CNS injury, ATP is released and contributes to the formation of reactive astrocytes, cells that produce molecules that can impede or promote axonal regeneration. Proliferation is one of the features of reactive astrogliosis, particularly in traumatic injury. Fibroblast growth factor (FGF)2 is also increased after injury and can stimulate astrocyte proliferation. Extracellular ATP enhances FGF2-induced proliferation in a process mediated by P2Y receptors and increased cyclin expression. However, when P2X receptors are activated, FGF2-induced proliferation is inhibited. P2 receptors are coupled to extracellular signal regulated protein kinase (ERK), and differences in the extent and duration of ERK activation by P2Y and P2X receptors may mediate the opposing effects of these receptors on FGF2-induced mitogenesis. Trauma also activates P2 receptor/ERK signalling, and stimulation of this and other protein kinase pathways by extracellular ATP increases expression of cell adhesion and extracellular matrix molecules involved in migration, glial contact formation, neuronal guidance and synapse formation. These findings support the hypothesis that purinergic signalling via protein kinase cascades plays a key role in astrocyte proliferation, glia–glia connections, and neuron–glia interactions in both normal and pathological conditions.