Abstract:
:There is clear evidence that an inflammatory reaction is mounted within the CNS following trauma, stroke, infection and seizures, thus augmenting brain damage. Furthermore, chronic inflammation of the CNS is implicated in many neurodegenerative disorders. However, the effects of products of inflammation on neuronal cells are poorly understood. Herein, we characterize the effects of a neurotoxic product of inflammation, prostaglandin J2 (PGJ2), on catechol-O-methyltransferase (COMT) in human dopaminergic-like neuroblastoma SK-N-SH cells and rat (P2) cortical neurons. COMT metabolizes catechols and catecholamines, a pathway relevant to neurodegeneration. PGJ2 treatment reduced the expression and activity of COMT, induced its sequestration into perinuclear aggregates and potentiated dopamine toxicity. The large COMT aggregates were co-localized with the centrosome, suggesting an aggresome-like structure. Our results indicate that COMT impairment induced by PGJ2 treatment may increase the concentration of dopamine (or its metabolites) to neurotoxic levels. Thus, COMT impairment following pro-inflammatory events may be a potential risk factor in neurodegeneration.
journal_name
Neurobiol Disjournal_title
Neurobiology of diseaseauthors
Ogburn KD,Bottiglieri T,Wang Z,Figueiredo-Pereira MEdoi
10.1016/j.nbd.2005.11.006keywords:
subject
Has Abstractpub_date
2006-05-01 00:00:00pages
294-301issue
2eissn
0969-9961issn
1095-953Xpii
S0969-9961(05)00312-8journal_volume
22pub_type
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