ArticleJournal of neurochemistry2012
Phosphodiesterase isoform-specific expression induced by traumatic brain injury.
Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- PDE4D: A Multipurpose Pharmacological Target.International journal of molecular sciences · 2024Review
- Therapeutic efficacy of rolipram delivered by PgP nanocarrier on secondary injury and motor function in a rat TBI model.Nanomedicine (London, England) · 2022Article
- The Emerging Role of Phosphodiesterases in Movement Disorders.Movement disorders : official journal of the Movement Disorder Society · 2021Review
- Preclinical Western Blot in the Era of Digital Transformation and Reproducible Research, an Eastern Perspective.Interdisciplinary sciences, computational life sciences · 2021Article
- Therapeutic Potential of Multifunctional Derivatives of Cholinesterase Inhibitors.Current neuropharmacology · 2021Article
- Ferroptosis-relevant mechanisms and biomarkers for therapeutic interventions in traumatic brain injury.Histology and histopathology · 2020Review
- Dominant-Negative Attenuation of cAMP-Selective Phosphodiesterase PDE4D Action Affects Learning and Behavior.International journal of molecular sciences · 2020Article
- Review
- A negative allosteric modulator of PDE4D enhances learning after traumatic brain injury.Neurobiology of learning and memory · 2018Article
- Cyclic nucleotide signaling changes associated with normal aging and age-related diseases of the brain.Cellular signalling · 2018Review
- East Indian Sandalwood Oil Is a Phosphodiesterase Inhibitor: A New Therapeutic Option in the Treatment of Inflammatory Skin Disease.Frontiers in pharmacology · 2018Article
- Therapeutic benefits of phosphodiesterase 4B inhibition after traumatic brain injury.PloS one · 2017Article
- Compartmentalized PDE4A5 Signaling Impairs Hippocampal Synaptic Plasticity and Long-Term Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Chronic Cognitive Dysfunction after Traumatic Brain Injury Is Improved with a Phosphodiesterase 4B Inhibitor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Traumatic Brain Injury Upregulates Phosphodiesterase Expression in the Hippocampus.Frontiers in systems neuroscience · 2016Article
- Treatment of traumatic brain injury with anti-inflammatory drugs.Experimental neurology · 2016Review
- Stability of rat models of fluid percussion-induced traumatic brain injury: comparison of three different impact forces.Neural regeneration research · 2015Article
- Phosphodiesterase-4 (PDE4) molecular pharmacology and Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015Review
- Phosphodiesterase inhibitors as therapeutics for traumatic brain injury.Current pharmaceutical design · 2015Review
- Inhibition of endogenous phosphodiesterase 7 promotes oligodendrocyte precursor differentiation and survival.Cellular and molecular life sciences : CMLS · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
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 PDE1A, PDE4B2, and PDE4D2, significantly increased from 30 min to 24 h post-injury. PDE10A significantly increased at 6 and 24 h after TBI. Phosphorylation of PDE4A significantly increased from 6 h to 7 days post-injury. In contrast, PDE1B, PD4A5, and PDE4A8 significantly decreased after TBI. No changes were observed with PDE1C, PDE3A, PDE4B1/3, PDE4B4, PDE4D3, PDE4D4, PDE8A, or PDE8B. Co-localization studies showed that PDE1A, PDE4B2, and phospho-PDE4A were neuronally expressed, whereas PDE4D2 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 PDE1A, PDE4B2, PDE4D2, or PDE10A.
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