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Purinergic receptor signaling regulates N‐cadherin expression in primary astrocyte cultures
Author(s) -
Tran Minh D.,
Wanner Ina B.,
Neary Joseph T.
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2008.05214.x
Subject(s) - purinergic receptor , microbiology and biotechnology , extracellular , biology , receptor , purinergic signalling , astrocyte , signal transduction , biochemistry , adenosine receptor , endocrinology , agonist , central nervous system
Extracellular ATP exerts both short‐term and long‐term effects in the CNS by stimulating cell‐surface purinergic receptors. Here we have examined the effect of purinergic receptor activation on N‐cadherin expression, a calcium‐dependent cell adhesion molecule involved in many processes, including glia‐glia and axon‐glia interactions. When primary cultures of rat cortical astrocytes were treated with ATP, N‐cadherin protein expression increased in a time‐ and concentration‐dependent manner. In addition, ATP treatment caused an increase in N‐cadherin immunoreactivity in both the cytoplasm and on the cell surface membrane. Interestingly, experiments with cycloheximide revealed that relocalization of N‐cadherin to the cell surface membrane were independent of protein synthesis. The ATP‐induced increase in N‐cadherin protein expression was blocked by reactive blue 2 and 8‐(p‐sulfophenyl)‐theophylline, suggesting involvement of both P2 and P1 purinergic receptors, respectively. In addition, N‐cadherin expression was partially blocked when signaling from purinergic receptors to extracellular signal regulated protein kinase or Akt was inhibited by 1,4‐diamino‐2,3‐dicyano‐1,4‐bis(2‐aminophenylthio)butadiene or wortmannin, respectively. By using an in vitro model of traumatic CNS injury, we found that N‐cadherin expression was increased when astrocytes were subjected to rapid and reversible mechanical strain. The findings presented here demonstrate a role for extracellular ATP, purinergic receptors and protein kinase signaling in regulating N‐cadherin expression and suggest a role for this mechanism in cell‐cell interactions.