Epigenetic regulation of Fgf1 transcription by CRTC1 and memory enhancement

Uchida, Shinichi; Shumyatsky, Gleb P.

doi:10.1016/j.brainresbull.2018.02.016

Cited by 13 publications

(9 citation statements)

References 138 publications

(200 reference statements)

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“…; Uchida et al . ; Uchida and Shumyatsky ,b). The non‐canonical pathway for CREB activation might therefore direct the differential expression of target genes that were not studied before.…”

Section: Discussionmentioning

confidence: 99%

Non‐canonical activation ofCREBmediates neuroprotection in aCaenorhabditis elegansmodel of excitotoxic necrosis

Feldmann

Chowdhury

Becker

et al. 2018

Journal of Neurochemistry

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Excitotoxicity, caused by exaggerated neuronal stimulation by Glutamate (Glu), is a major cause of neurodegeneration in brain ischemia. While we know that neurodegeneration is triggered by overstimulation of Glu‐receptors (GluRs), the subsequent mechanisms that lead to cellular demise remain controversial. Surprisingly, signaling downstream of GluRs can also activate neuroprotective pathways. The strongest evidence involves activation of the transcription factor cAMP response element‐binding protein (CREB), widely recognized for its importance in synaptic plasticity. Canonical views describe CREB as a phosphorylation‐triggered transcription factor, where transcriptional activation involves CREB phosphorylation and association with CREB‐binding protein. However, given CREB's ubiquitous cross‐tissue expression, the multitude of cascades leading to CREB phosphorylation, and its ability to regulate thousands of genes, it remains unclear how CREB exerts closely tailored, differential neuroprotective responses in excitotoxicity. A non‐canonical, alternative cascade for activation of CREB‐mediated transcription involves the CREB co‐factor cAMP‐regulated transcriptional co‐activator (CRTC), and may be independent of CREB phosphorylation. To identify cascades that activate CREB in excitotoxicity we used a Caenorhabditis elegans model of neurodegeneration by excitotoxic necrosis. We demonstrated that CREB's neuroprotective effect was conserved, and seemed most effective in neurons with moderate Glu exposure. We found that factors mediating canonical CREB activation were not involved. Instead, phosphorylation‐independent CREB activation in nematode excitotoxic necrosis hinged on CRTC. CREB‐mediated transcription that depends on CRTC, but not on CREB phosphorylation, might lead to expression of a specific subset of neuroprotective genes. Elucidating conserved mechanisms of excitotoxicity‐specific CREB activation can help us focus on core neuroprotective programs in excitotoxicity. Cover Image for this issue: doi: .

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Section: Discussionmentioning

confidence: 99%

Non‐canonical activation ofCREBmediates neuroprotection in aCaenorhabditis elegansmodel of excitotoxic necrosis

Feldmann

Chowdhury

Becker

et al. 2018

Journal of Neurochemistry

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“…Calcium-signaling activation further sends its signal toward downstream epigenetic and transcription modulators, such as MEF2, MeCP2, and HDAC5. These pathways modulate gene expression that affects dendritic growth, synaptic development, and neuronal plasticity ( Greer and Greenberg, 2008 ; Graff and Tsai, 2013 ; Takemoto-Kimura et al, 2017 ; Uchida and Shumyatsky, 2018a , b ; Figure 1 ). Taken together, calcium-signaling stimulation through NMDARs and/or AMPARs activates multiple downstream nucleocytoplasmic pathways; it induces activity-dependent epigenetic genetic expression, contributing to depression and antidepressant action.…”

Section: The Glutamatergic System In Neuroplasticity Intracellular Signaling and Gene Expressionmentioning

confidence: 99%

A Multiscale View of the Mechanisms Underlying Ketamine’s Antidepressant Effects: An Update on Neuronal Calcium Signaling

Kawatake-Kuno

Murai

Uchida

2021

Front. Behav. Neurosci.

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Major depressive disorder (MDD) is a debilitating disease characterized by depressed mood, loss of interest or pleasure, suicidal ideation, and reduced motivation or hopelessness. Despite considerable research, mechanisms underlying MDD remain poorly understood, and current advances in treatment are far from satisfactory. The antidepressant effect of ketamine is among the most important discoveries in psychiatric research over the last half-century. Neurobiological insights into the ketamine’s effects have shed light on the mechanisms underlying antidepressant efficacy. However, mechanisms underlying the rapid and sustained antidepressant effects of ketamine remain controversial. Elucidating such mechanisms is key to identifying new therapeutic targets and developing therapeutic strategies. Accumulating evidence demonstrates the contribution of the glutamatergic pathway, the major excitatory neurotransmitter system in the central nervous system, in MDD pathophysiology and antidepressant effects. The hypothesis of a connection among the calcium signaling cascade stimulated by the glutamatergic system, neural plasticity, and epigenetic regulation of gene transcription is further supported by its associations with ketamine’s antidepressant effects. This review briefly summarizes the potential mechanisms of ketamine’s effects with a specific focus on glutamatergic signaling from a multiscale perspective, including behavioral, cellular, molecular, and epigenetic aspects, to provide a valuable overview of ketamine’s antidepressant effects.

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“…All in all, acute intravenous administration of FGF-1 may become a new way for the treatment of PSCI in the future. Also, a genetic study revealed that FGF-1 may be involved in AD due to the obvious association of single nucleotide polymorphisms in FGF-1 gene, and the number of FGF-1-immunolabeled neurons decreases in AD patients, indicating that FGF-1 deficiency may be related to the pathophysiology of AD [21]. The increase of FGF-1 levels exerts a significant effect on glial cells and capillary proliferation, neurite outgrowth, and synapse formation.…”

Section: The Effects Of Fgfs On Psci Fgf-1 (Afgf)mentioning

confidence: 99%

Progress on the study of fibroblast growth factors as novel therapeutics in post-stroke cognitive impairment

Fan²

2021

APT

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Post-stroke cognitive impairment (PSCI) is one of the most common complications after stroke, which severely affects the daily life abilities and social function of patients. Fibroblast growth factor (FGF), as a regulator of homeostasis, participates in the regulation of cell metabolism and hormone secretion, and can increase cerebral blood flow and promote nerve repair which improves PSCI. Here, we will conduct a review on the typing, characteristics, and mechanism of action of FGF to further understand its function and mechanism in PSCI

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Epigenetic regulation of Fgf1 transcription by CRTC1 and memory enhancement

Cited by 13 publications

References 138 publications

Non‐canonical activation ofCREBmediates neuroprotection in aCaenorhabditis elegansmodel of excitotoxic necrosis

Non‐canonical activation ofCREBmediates neuroprotection in aCaenorhabditis elegansmodel of excitotoxic necrosis

A Multiscale View of the Mechanisms Underlying Ketamine’s Antidepressant Effects: An Update on Neuronal Calcium Signaling

Progress on the study of fibroblast growth factors as novel therapeutics in post-stroke cognitive impairment

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