Adenosine Kinase Expression Modulates Expression of Myelin Proteolipid Protein

Wu, Natalie Lai-man; Boison, Detlev

doi:10.2174/1874082000701010015

TONEURJ

2007

DOI: 10.2174/1874082000701010015

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Adenosine Kinase Expression Modulates Expression of Myelin Proteolipid Protein

Natalie Lai-man Wu¹,

Detlev Boison²

Abstract: Abstract:Adenosine is known to regulate myelination in vitro. Here we tested the hypothesis that adenosine, regulated by adenosine kinase (ADK), might regulate myelin-specific protein expression and myelination in vivo. We demonstrate that transgenic overexpression of ADK, which reduces adenosine in mouse brain, results in increased levels of myelin proteolipid protein.

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Cited by 2 publications

References 21 publications

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Role of adenosine kinase in cochlear development and response to noise

Vlajkovic

Guo

Dharmawardana

et al. 2010

J of Neuroscience Research

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Adenosine signalling has an important role in cochlear protection from oxidative stress. In most tissues, intracellular adenosine kinase (ADK) is the primary route of adenosine metabolism and the key regulator of intracellular and extracellular adenosine levels. The present study provides the first evidence for ADK distribution in the adult and developing rat cochlea. In the adult cochlea ADK was localised to the nuclear or perinuclear region of spiral ganglion neurones, lateral wall tissues and epithelial cells lining scala media. In the developing cochlea, ADK was strongly expressed in multiple cell types at birth, and reached its peak level of expression at postnatal day 21 (P21). Ontogenetic changes in ADK expression were evident in the spiral ganglion, organ of Corti and stria vascularis. In the spiral ganglion, ADK showed a shift from predominantly satellite cell immunolabelling at P1 to neuronal expression from P14 onwards. In contrast to the role of ADK in various aspects of cochlear development, ADK contribution to the cochlear response to noise stress was less obvious. Transcript and protein levels of ADK were unaltered in the cochlea exposed to broadband noise (90–110dBSPL, 24 hours) and the selective inhibition of ADK in the cochlea with ABT-702 failed to restore hearing thresholds after exposure to traumatic noise. This study indicates that ADK is involved in purine salvage pathways for nucleotide synthesis in the adult cochlea, but its role in the regulation of adenosine signalling under physiological and pathological conditions is yet to be established.

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Role of adenosine kinase in cochlear development and response to noise

Vlajkovic

Guo

Dharmawardana

et al. 2010

J of Neuroscience Research

Self Cite

View full text Add to dashboard Cite

show abstract

Adenosine dysfunction in astrogliosis: cause for seizure generation?

et al. 2007

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Epilepsy is characterized by both neuronal and astroglial dysfunction. The endogenous anticonvulsant adenosine, the level of which is largely controlled by astrocytes, might provide a critical link between astrocyte and neuron dysfunction in epilepsy. Here we studied astrogliosis, a hallmark of the epileptic brain, adenosine dysfunction and the emergence of spontaneous seizures in a comprehensive approach including a new mouse model of focal epileptogenesis, mutant mice with altered brain levels of adenosine, and mice lacking adenosine A 1 receptors. In wild type mice, following a focal epileptogenesis-precipitating injury, astrogliosis, upregulation of the adenosineremoving astrocytic enzyme adenosine kinase (ADK), and spontaneous seizures all coincided in a spatio-temporally restricted manner. Importantly, these spontaneous seizures were mimicked in untreated transgenic mice overexpressing ADK in brain or those lacking A 1 receptors. Conversely, mice with reduced forebrain ADK did not develop astrogliosis or spontaneous seizures. Our studies define ADK as critical upstream regulator of A 1 receptor mediated modulation of neuronal excitability and support the ADK hypothesis of epileptogenesis implicating that upregulation of ADK during astrogliosis provides a critical link between astrocyte and neuron dysfunction in epilepsy. These findings define ADK as rational target for therapeutic intervention.

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Adenosine Kinase Expression Modulates Expression of Myelin Proteolipid Protein

Cited by 2 publications

References 21 publications

Role of adenosine kinase in cochlear development and response to noise

Role of adenosine kinase in cochlear development and response to noise

Adenosine dysfunction in astrogliosis: cause for seizure generation?

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