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Phosphodiesterase isoform‐specific expression induced by traumatic brain injury
Author(s) -
Oliva Anthony A.,
Kang Yuan,
Furones Concepcion,
Alonso Ofelia F.,
Bruno Olga,
Dietrich W. Dalton,
Atkins Coleen M.
Publication year - 2012
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/jnc.12049
Subject(s) - traumatic brain injury , phosphodiesterase , inflammation , medicine , endocrinology , cortex (anatomy) , biology , neuroscience , biochemistry , enzyme , psychiatry
Traumatic brain injury ( TBI ) results in significant inflammation which contributes to the evolving pathology. Previously, we have demonstrated that cyclic AMP ( cAMP ), a molecule involved in inflammation, is down‐regulated after TBI . To determine the mechanism by which cAMP is down‐regulated after TBI , we determined whether TBI induces changes in phosphodiesterase ( PDE ) expression. Adult male Sprague Dawley rats received moderate parasagittal fluid‐percussion brain injury ( FPI ) or sham injury, and the ipsilateral, parietal cortex was analyzed by western blotting. In the ipsilateral parietal cortex, expression of PDE 1A, PDE 4B2, and PDE 4D2, significantly increased from 30 min to 24 h post‐injury. PDE10A significantly increased at 6 and 24 h after TBI . Phosphorylation of PDE 4A significantly increased from 6 h to 7 days post‐injury. In contrast, PDE 1B, PD 4A5, and PDE 4A8 significantly decreased after TBI . No changes were observed with PDE 1C, PDE 3A, PDE 4B1/3, PDE 4B4, PDE 4D3, PDE 4D4, PDE 8A, or PDE 8B. Co‐localization studies showed that PDE 1A, PDE 4B2, and phospho‐ PDE 4A were neuronally expressed, whereas PDE 4D2 was expressed in neither neurons nor glia. These findings suggest that therapies to reduce inflammation after TBI could be facilitated with targeted therapies, in particular for PDE 1A, PDE 4B2, PDE 4D2, or PDE 10A.