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CircAkt3 participates in bone cancer pain progression in rats by modulating MAPK signalling pathway

ABSTRACT: CircAkt3 participates in bone cancer pain progression in rats by modulating MAPK signalling pathway

PROVIDER: PRJNA933211 | ENA |

REPOSITORIES: ENA

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CircAkt3 participates in bone cancer pain progression in rats by modulating MAPK signalling pathway

Project description:CircAkt3 participates in bone cancer pain progression in rats by modulating MAPK signalling pathway

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CircAkt3 participates in bone cancer pain progression in rats by modulating MAPK signalling pathway

Project description:CircRNA parent genes were mainly enriched in MAPK and neurodevelopmental signalling pathways. CircAkt3 and circMap4k1 were significantly up-regulated in the bone cancer pain group. CircaAkt3 may increase p-ERK expression by upregulating Col8a1, which may further activate the MAPK pathway.

2023-02-14 | GSE224978 | GEO

CircAkt3 participates in bone cancer pain progression in rats by modulating MAPK signalling pathway

Project description:CircRNA parent genes were mainly enriched in MAPK and neurodevelopmental signalling pathways. CircAkt3 and circMap4k1 were significantly up-regulated in the BCP group. CircaAkt3 may increase p-ERK expression by upregulating Col8a1, which may further activate the MAPK pathway.

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Project description:MAPK

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FEZ1 participates in human embryonic brain development by modulating neuronal progenitor subpopulation specification and migration

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DREAM in pain mechanisms in the trigeminal ganglia

Project description:Expression of DREAM in dorsal root ganglia and spinal cord is related to endogenous control mechanisms of acute and chronic pain. In primary sensory trigeminal neurons high levels of endogenous DREAM protein are preferentially localized in the nucleus, suggesting a major transcriptional role. Here, we show that DREAM participates in the control of trigeminal pain perception through the regulation of prodynorphin and BDNF. Furthermore, genome-wide analysis of trigeminal neurons in daDREAM transgenic mice revealed that cathepsin L (CTSL) and the monoglyceride lipase (MGLL) are new DREAM downstream targets and have a role in the regulation of trigeminal nociception.

2016-04-22 | GSE69619 | GEO

The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment.

Project description:The Role of KDM2A and H3K36me2 Demethylation in Modulating MAPK Signaling during Neurodevelopment.

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Ventral hippocampal CA1 modulates pain behaviors in mice with peripheral inflammation

Project description:Chronic pain is one of the most significant and costly medical problems throughout the world. Recent evidence has confirmed the hippocampus as an active modulator of pain chronicity but the underlying mechanisms remain poorly defined. By means of in vivo electrophysiology together with chemogenetic and optogenetic manipulations in freely behaving mice, we identified a neural ensemble in the ventral hippocampal CA1 (vCA1) that showed inhibitory responses to noxious external stimuli, but not to innocuous stimuli. Following peripheral inflammation, this neuronal ensemble became responsive to innocuous stimuli and causally contributed to sensory hypersensitivity in inflammatory animals. Mimicking this inhibition of vCA1 neurons using chemogenetics in naïve mice induced chronic pain-like behavioral changes, whereas activating these vCA1 neurons in mice with chronic peripheral inflammation resulted in a striking reduction of pain-related behaviors. Pathway-specific manipulation of vCA1 projections to the basolateral amygdala (BLA) and infralimbic cortex (IL) showed that these pathways were differentially involved in pain modulation at different temporal stages of chronic inflammatory pain. These results confirm a crucial role of the ventral hippocampus and its circuits in modulating the development of chronic pain in mice.

2022-12-19 | PXD038416 | Pride

NIS-lncRNA promotes neuropathic pain by increasing Ccl2 expression

Project description:Maladaptive changes of nerve injury–associated genes in dorsal root ganglia (DRGs) are critical for neuropathic pain genesis. Emerging evidence supports the role of long noncoding RNAs (lncRNAs) in regulating gene transcription. Here we identified a conserved lncRNA, named nerve injury–specific lncRNA (NIS-lncRNA) for its upregulation in injured DRGs exclusively in response to nerve injury. This upregulation was triggered by nerve injury–induced increase in DRG ELF1, a transcription factor that bound to the NIS-lncRNA promoter. Blocking this upregulation attenuated nerve injury–induced CCL2 increase in injured DRGs and nociceptive hypersensitivity during the development and maintenance periods of neuropathic pain. Mimicking NIS-lncRNA upregulation elevated CCL2 expression, increased CCL2-mediated excitability in DRG neurons, and produced neuropathic pain symptoms. Mechanistically, NIS-lncRNA recruited more binding of the RNA-interacting protein FUS to the Ccl2 promoter and augmented Ccl2 transcription in injured DRGs. Thus, NIS-lncRNA participates in neuropathic pain likely by promoting FUS-triggered DRG Ccl2 expression and may be a potential target in neuropathic pain management.

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Genomics of Pain - Resilience to Pain

Project description:Genomics of Pain - Resilience to Pain

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