TNF-α Preconditioning Protects Neurons via Neuron-Specific Up-Regulation of CREB-Binding Protein

Saha, Ramendra N.; Ghosh, Alip; Palencia, Carlos A.; Fung, Yiu K.; Dudek, Serena M.; Pahan, Kalipada

doi:10.4049/jimmunol.0801892

Cited by 54 publications

(47 citation statements)

References 60 publications

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“…Hippocampal neurons were isolated from fetuses (E18) of pregnant female mice as described by us (Jana et al, 2007; Saha et al, 2009). Briefly, dissection and isolation procedures were performed in an ice-cold, sucrose buffer solution (sucrose 0.32 M, Tris 0.025 M; pH 7.4).…”

Section: Methodsmentioning

confidence: 99%

Cinnamon Converts Poor Learning Mice to Good Learners: Implications for Memory Improvement

Modi

Rangasamy

Dasarathi

et al. 2016

J Neuroimmune Pharmacol

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This study underlines the importance of cinnamon, a commonly used natural spice and flavoring material, and its metabolite sodium benzoate (NaB) in converting poor learning mice to good learning ones. NaB, but not sodium formate, was found to upregulate plasticity-related molecules, stimulate NMDA- and AMPA-sensitive calcium influx and increase of spine density in cultured hippocampal neurons. NaB induced the activation of CREB in hippocampal neurons via protein kinase A (PKA), which was responsible for the upregulation of plasticity-related molecules. Finally, spatial memory consolidation-induced activation of CREB and expression of different plasticity-related molecules were less in the hippocampus of poor learning mice as compared to good learning ones. However, oral treatment of cinnamon and NaB increased spatial memory consolidation-induced activation of CREB and expression of plasticity-related molecules in the hippocampus of poor-learning mice and converted poor learners into good learners. These results describe a novel property of cinnamon in switching poor learners to good learners via stimulating hippocampal plasticity.

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Section: Methodsmentioning

confidence: 99%

Cinnamon Converts Poor Learning Mice to Good Learners: Implications for Memory Improvement

Modi

Rangasamy

Dasarathi

et al. 2016

J Neuroimmune Pharmacol

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“…6D). Evidence suggests that TNF-a is an upstream inducer of DNA binding activity of CREB and C/EBP-b (Saha et al, 2009;Wang et al, 2010). The DNA-protein complex formed with CREB and C/EBP-b in JEV-infected microglia decreased in the presence of TNF-a neutralizing antibody.…”

Section: C/ebp-b and Creb Contributed To Jev-induced Glutaminase Exprmentioning

confidence: 99%

Glutamate released by Japanese encephalitis virus‐infected microglia involves TNF‐α signaling and contributes to neuronal death

Chen

Chang

et al. 2011

Glia

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The substantial activation of microglia in Japanese encephalitis virus (JEV)-induced Japanese encephalitis found in numerous studies demonstrates that the disease pathogenesis involves bystander damage caused by microglia-released mediators. Previously, we reported that microglia synthesized and secreted bioactive mediators with neurotoxic potential into the cultured supernatants in response to JEV infection. In this study, we found that the supernatants of JEV-infected microglia caused MK801-inhibitable neuronal damage in cultured neurons, indicating a potential excitotoxic mechanism. Infection with JEV was found to elicit the extracellular glutamate accumulation from microglia but not from neuron and astrocyte cultures. The glutaminase inhibitor 6-diazo-5-oxo-L-norleucine, cystine/glutamate antiporter inhibitor α-aminoadipic acid, and the gap junction inhibitor carbenoxolone reduced JEV infection-induced microglial glutamate release and neurotoxicity. We further demonstrated that tumor necrosis factor-alpha (TNF-α) was a key cytokine which stimulated extensive microglial glutamate release by up-regulating glutaminase expression via signals involving protein kinase C, cAMP responsive element-binding protein, and CAAT-enhancer-binding protein-beta. Although the elevated expression of excitatory amino acid transporter 1 and 2 was observed in JEV-infected cells, the glutamate uptake activity was significantly inhibited by TNF-α. The JEV infection-induced alterations, such as the extracellular glutamate release and glutamate-mediated excitoneurotoxicity, also occurred in neuron/glia cultures. Our findings support a potential link between neuroinflammation and the development of excitotoxic neuronal injury in Japanese encephalitis. The link between neuroinflammation and excitotoxic death may involve a mechanism in which TNF-α released by microglia plays a facilitory role in glutamate excitoneurotoxicity via up-regulation of glutamate synthesis and down-regulation of glutamate uptake.

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“…Indeed, drugs targeted to increase specific CBP expression could reach the threshold of CBP molecules necessary to activate correct genetic programs with more precisions than solely modulating histone acetylation levels. Pharmacological modulation of CBP levels has been reported recently (Saha et al, 2009): preconditioning of neurons with TNF-a protected them from degenerative conditions (and particularly Ab toxicity) through a neuron-specific increase of CBP expression. The authors suggested that an 'adequate' amount of CBP is required at a basal level to ensure pro-survival functions.…”

Section: Cbp Expression and Sensitivity In Neuronal Functionsmentioning

confidence: 99%

Spatial Memory Consolidation is Associated with Induction of Several Lysine-Acetyltransferase (Histone Acetyltransferase) Expression Levels and H2B/H4 Acetylation-Dependent Transcriptional Events in the Rat Hippocampus

Bousiges

Vasconcelos

Neidl

et al. 2010

Neuropsychopharmacol

161

142

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Numerous genetic studies have shown that the CREB-binding protein (CBP) is an essential component of long-term memory formation, through its histone acetyltransferase (HAT) function. E1A-binding protein p300 and p300/CBP-associated factor (PCAF) have also recently been involved in memory formation. By contrast, only a few studies have reported on acetylation modifications during memory formation, and it remains unclear as to how the system is regulated during this dynamic phase. We investigated acetylation-dependent events and the expression profiles of these HATs during a hippocampus-dependent task taxing spatial reference memory in the Morris water maze. We found a specific increase in H2B and H4 acetylation in the rat dorsal hippocampus, while spatial memory was being consolidated. This increase correlated with the degree of specific acetylated histones enrichment on some memory/plasticity-related gene promoters. Overall, a global increase in HAT activity was measured during this memory consolidation phase, together with a global increase of CBP, p300, and PCAF expression. Interestingly, these regulations were altered in a model of hippocampal denervation disrupting spatial memory consolidation, making it impossible for the hippocampus to recruit the CBP pathway (CBP regulation and acetylated-H2B-dependent transcription). CBP has long been thought to be present in limited concentrations in the cells. These results show, for the first time, that CBP, p300, and PCAF are dynamically modulated during the establishment of a spatial memory and are likely to contribute to the induction of a specific epigenetic tagging of the genome for hippocampus-dependent (spatial) memory consolidation. These findings suggest the use of HAT-activating molecules in new therapeutic strategies of pathological aging, Alzheimer's disease, and other neurodegenerative disorders.

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TNF-α Preconditioning Protects Neurons via Neuron-Specific Up-Regulation of CREB-Binding Protein

Cited by 54 publications

References 60 publications

Cinnamon Converts Poor Learning Mice to Good Learners: Implications for Memory Improvement

Cinnamon Converts Poor Learning Mice to Good Learners: Implications for Memory Improvement

Glutamate released by Japanese encephalitis virus‐infected microglia involves TNF‐α signaling and contributes to neuronal death

Spatial Memory Consolidation is Associated with Induction of Several Lysine-Acetyltransferase (Histone Acetyltransferase) Expression Levels and H2B/H4 Acetylation-Dependent Transcriptional Events in the Rat Hippocampus

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