Regulation of DREAM Expression by Group I mGluR

Lee, Jinu; Kim, Insook; Oh, Seung Joon; Ko, Suk Jin; Lim, Mi Kyung; Kim, Dong Goo; Kim, Chul Hoon

doi:10.4196/kjpp.2011.15.2.95

Cited by 3 publications

(3 citation statements)

References 25 publications

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“…Intriguingly, this analgesic effect was not accompanied by deficits in motor function, learning or memory, and immune and cardiac functions as it occurs in opioid treatments [14]. In addition, the activation of mGluR5 causes an increase in the protein stability of DREAM, contributing to the pronociceptive role of this metabotropic glutamate receptor [21]. For these reasons, the pharmacological inhibition of DREAM may represent an interesting new analgesic strategy for the treatment of pain because of the lack of typical side-effects of opioids.…”

Section: Dream and Neuropathic Painmentioning

confidence: 89%

“…For instance, DREAM inhibits c-fos transcription as a consequence of the rise in [Ca 2+ ] n following glutamate stimulation in neurons [1]. Furthermore, the stimulation of group I metabotropic glutamate receptors 1 and 5 (mGluR1/5) positively increases the neuronal levels of DREAM [21], thus reinforcing its transcriptional inhibition. By contrast, glutamate stimulation in astrocytes causes the nuclear export of DREAM, thus relieving transcription inhibition of its target genes [22].…”

Section: Control Of Gene Expression By Dream In the Nucleusmentioning

confidence: 99%

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Emerging Role of DREAM in Healthy Brain and Neurological Diseases

Molinaro

Sanguigno

Casamassa³

et al. 2023

IJMS

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The downstream regulatory element antagonist modulator (DREAM) is a multifunctional Ca2+-sensitive protein exerting a dual mechanism of action to regulate several Ca2+-dependent processes. Upon sumoylation, DREAM enters in nucleus where it downregulates the expression of several genes provided with a consensus sequence named dream regulatory element (DRE). On the other hand, DREAM could also directly modulate the activity or the localization of several cytosolic and plasma membrane proteins. In this review, we summarize recent advances in the knowledge of DREAM dysregulation and DREAM-dependent epigenetic remodeling as a central mechanism in the progression of several diseases affecting central nervous system, including stroke, Alzheimer’s and Huntington’s diseases, amyotrophic lateral sclerosis, and neuropathic pain. Interestingly, DREAM seems to exert a common detrimental role in these diseases by inhibiting the transcription of several neuroprotective genes, including the sodium/calcium exchanger isoform 3 (NCX3), brain-derived neurotrophic factor (BDNF), pro-dynorphin, and c-fos. These findings lead to the concept that DREAM might represent a pharmacological target to ameliorate symptoms and reduce neurodegenerative processes in several pathological conditions affecting central nervous system.

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Section: Dream and Neuropathic Painmentioning

confidence: 89%

Section: Control Of Gene Expression By Dream In the Nucleusmentioning

confidence: 99%

Emerging Role of DREAM in Healthy Brain and Neurological Diseases

Molinaro

Sanguigno

Casamassa³

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

“…Other glutamate receptors, such as the metabotropic glutamate receptor (mGluR), also became dominant after inhibition of the NMDA receptor in this study, contributing to the upregulation of the DREAM protein level in the nuclear compartment. The group 1 mGluR has been reported to regulate DREAM protein activity in neurons [33]. …”

Section: Discussionmentioning

confidence: 99%

The Effects of Pre-emptive Administration of Ketamine and norBNI on Pain Behavior, c-Fos, and Prodynorphin Protein Expression in the Rat Spinal Cord after Formalin-induced Pain Is Modulated by the DREAM Protein

2013

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BackgroundWe investigated the effects of pre-emptive administration of ketamine and norBNI on pain behavior and the expression of DREAM, c-Fos, and prodynorphin proteins on the ipsilateral side of the rat spinal cord at 2 and 4 hours after formalin injection.MethodsEighty-four male Sprague Dawley rats were divided into 4 major groups consisting of control rats (C) (n = 12), rats given only formalin injections (F) (n = 24), and rats treated with pre-emptive administration of either ketamine (K+F) (n = 24) or norBNI (N+F) (n = 24). The non-control groups were further divided into subgroups consisting of rats that were sacrificed at 2 and 4 hours (n = 12 for each group) after formalin injection. Pain behavior was recorded for 1 hour. After 2 and 4 hours, the rats were sacrificed and the spinal cords (L4-L5 sections) were removed for immunohistochemistry and Western blot analysis.ResultsThe pain behavior response was reduced in the K+F group compared to the other groups during the second phase of the formalin pain response. We detected an increase in the nuclear DREAM protein level in the K+F group at 2 and 4 hours and a transient decrease in the N+F group at 2 hours; however, it increased at 4 hours after injection. Fos-like immunoreactivity (FLI) and Prodynorphin-like immunoreactivity (PLI) neurons decreased in the K+F group but increased in the N+F group at 2 hours after injection. While FLI decreased, PLI increased in all groups at 4 hours after injection.ConclusionsWe suggest that NMDA and kappa opioid receptors can modulate DREAM protein expression, which can affect pain behavior and protein transcriptional processes at 2 hours and bring about either harmful or protective effects at 4 hours after formalin injection.

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TRPC-Mediated Current Is Not Involved in Endocannabinoid-Induced Short-Term Depression in Cerebellum

Chang

Park

Kim

et al. 2012

Korean J Physiol Pharmacol

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It has been reported that activation of metabotropic glutamate receptor 1 (mGluR1) can mediate endocannabinoid-induced short-term depression of synaptic transmission in cerebellar parallel fiber (PF)-Purkinje cell (PC) synapse. mGluR1 has signaling pathways involved in intracellular calcium increase which may contribute to endocannabinoid release. Two major mGluR1-evoked calcium signaling pathways are known: (1) slow-kinetic inward current carried by transient receptor potential canonical (TRPC) channel which is permeable to Ca2+; (2) IP3-induced calcium release from intracellular calcium store. However, it is unclear how much each calcium source contributes to endocannabinoid signaling. Here, we investigated whether calcium influx through mGluR1-evoked TRPC channel contributes to endocannabinoid signaling in cerebellar Purkinje cells. At first, we applied SKF96365 to inhibit TRPC, which blocked endocannabinoid-induced short-term depression completely. However, an alternative TRP channel inhibitor, BTP2 did not affect endocannabinoid-induced short-term depression although it blocked mGluR1-evoked TRPC currents. Endocannabinoid signaling occurred normally even though the TRPC current was mostly blocked by BTP2. Our data imply that TRPC current does not play an important role in endocannabinoid signaling. We also suggest precaution in applying SKF96365 to inhibit TRP channels and propose BTP2 as an alternative TRPC inhibitor.

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Regulation of DREAM Expression by Group I mGluR

Cited by 3 publications

References 25 publications

Emerging Role of DREAM in Healthy Brain and Neurological Diseases

Emerging Role of DREAM in Healthy Brain and Neurological Diseases

The Effects of Pre-emptive Administration of Ketamine and norBNI on Pain Behavior, c-Fos, and Prodynorphin Protein Expression in the Rat Spinal Cord after Formalin-induced Pain Is Modulated by the DREAM Protein

TRPC-Mediated Current Is Not Involved in Endocannabinoid-Induced Short-Term Depression in Cerebellum

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