Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Rimegepant treatment on gene expression in the trigeminal ganglion of mice on the tumor-transplanted side.

ABSTRACT: The trigeminal nerve is primarily responsible for facial sensation and exhibits the highest expression of CGRP. Here, we explored the impact of Rimegepant on the transcriptome of the trigeminal ganglion in mice and found that the transcription profiles changed significantly following treatment compared to the control group. Following Rimegepant administration, we observed a significant downregulation of innate immune-related items within the trigeminal ganglia, as well as functional items directly associated with pain perception and calcium signaling pathways.The activation of innated immune within the trigeminal ganglia is known to enhance nociceptive responses, which were also directly linked to the activation of calcium signaling pathways. These results suggest that Rimegepant alleviates OSCC-related pain by mitigating the inflammatory condition within the trigeminal ganglion. We then categorized the genes enriched in these functional groups. Genes that promote the proliferation and differentiation of innate immune cells, and those related to the expression of proinflammatory mediators, were significantly downregulated, while those associated with anti-inflammatory functions were significantly upregulated. Additionally, genes from various chemokine receptor families and ion channel genes linked to neuronal activity were significantly downregulated. Collectively, these results suggest that CGRP influences OSCC-related pain by modulating the innate immune status of the trigeminal nerve.

ORGANISM(S): Mus musculus

PROVIDER: GSE260740 | GEO | 2026/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Anti-CGRP Monoclonal Antibodies Counteract Interoceptive Awareness of Malaise

Project description:Study of the expression profiles of brain regions (amygdala, hippocampus and cerebral cortex) and trigeminal ganglia collected from rats treated with fremanezumab, an anti-calcitonin gene related peptide (CGRP) mAb, used for the prevention of migraine.

2024-05-30 | E-MTAB-13507 | biostudies-arrayexpress

Human and mouse trigeminal ganglia cell atlas implicates multiple cell types in migraine

Project description:The sensitization of trigeminal ganglion neurons contributes to primary headache disorders such as migraine, but the specific neuronal and non-neuronal trigeminal subtypes involved remain unclear. We thus developed a cell atlas in which human and mouse trigeminal ganglia are transcriptionally and epigenomically profiled at single-cell resolution. These data describe evolutionarily conserved and human-specific gene expression patterns within each trigeminal ganglion cell type, as well as the transcription factors and gene regulatory elements that contribute to cell-type-specific gene expression. We then leverage these data to identify trigeminal ganglion cell types that are implicated both by human genetic variation associated with migraine and two mouse models of headache. This trigeminal ganglion cell atlas improves our understanding of the cell types, genes, and epigenomic features involved in headache pathophysiology and establishes a rich resource of cell-type-specific molecular features to guide the development of more selective treatments for headache and facial pain.

2022-02-26 | GSE197289 | GEO

CGRP signaling Links Tumor-Associated Pain to Immune Evasion in Oral Squamous Cell Carcinoma

Project description:Peripheral sensory nerves are thought to contribute to solid tumor growth, particularly in oral squamous cell carcinoma (OSCC); however, the link between pain and immunosuppression remains unresolved. Here, using a prospective observational study, we demonstrate an inverse relationship between OSCC-induced pain mediated by calcitonin gene-related peptide (CGRP)-expressing nerves and tumor-associated immunity. Bulk RNA sequencing of tumor-innervating sensory neurons from mice revealed differential regulation of genes associated with excitability, neurotransmission, and axonal sprouting. Using a gain-of-function approach with persistent stimulation of peptidergic afferents, we show that sensory neurons promote oral tongue tumor growth and limit the activation of effective anti-tumor immune responses via efferent CGRP release. Conversely, loss-of-function approaches—including local ablation of nociceptive nerves and systemic CGRP receptor antagonism—slowed tumor growth and improved anti-tumor immunity. Targeting CGRP may therefore represent a therapeutic strategy in OSCC to reduce pain and improve treatment response.

2026-01-19 | GSE315799 | GEO

Gene modulation in acetic acid-induced oral ulcerative mucositis

Project description:To reveal the molecular mechanisms underlying oral ulcerative mucositis-induced pain, we investigated putative pain-associated mediators, pain-related behaviors and gene modulation in a rat oral mucositis model. On day 1 after acetic acid treatment, the mucosal area showed slight redness and swelling but no evidence of ulceration or pain induction. On day 2, oral ulcers were obvious, as was the induction of spontaneous and mechanical pain. In the treated mucosal area, bacterial loading and prostaglandin E2 increased beginning on day 2; no significant changes were observed on day 1. DNA microarray analysis of trigeminal ganglion tissue collected on day 2 identified 32 significantly regulated genes (>1.5-fold change in expression). The up-regulation of the top 3 genes, Hamp (hepcidin antimicrobial peptide), Reg3b (regenerating islet-derived 3Î²) and Serpina3n (serine peptidase inhibitor A3N), was validated through quantitative RT-PCR. Systemic antibiotic pre-treatment did not increase the mRNA levels. Therefore, we conclude that the oral ulcerative mucositis-induced pain is caused by infectious inflammation of the ulcerative area and stimulates anti-bacterial and anti-peptidase gene expressions in sensory neurons. Oral ulcerative mucositis-induced gene expression in trigeminal ganglion tissue was measured. Ten Wistar rats were divided into the following two groups, control, oral ulcerative mucositis (stomatitis). Five rats were anesthetized with sodium pentobarbital. A piece of filter paper was soaked in 50% acetic acid diluted with water and placed in the labial fornix region of the inferior incisors of rats for 30 sec. Other five rats received only anesthesia without any treatment were used as a control. On day 2 after acetic acid treatment, oral ulcerative mucositis was obvious and trigeminal ganglion tissues in two groups were collected for DNA microarray analysis.

2016-06-15 | E-GEOD-83349 | biostudies-arrayexpress

The transcriptional landscape of the developing chick trigeminal ganglion

Project description:The trigeminal ganglion is a critical structure in the peripheral nervous system, responsible for transmitting sensations of touch, pain, and temperature from craniofacial regions to the brain. Trigeminal ganglion development depends upon intrinsic cellular programming as well as extrinsic signals exchanged by diverse cell populations. With its complex anatomy and dual cellular origin from cranial placodes and neural crest cells, the trigeminal ganglion offers a rich context for examining diverse biological processes, including cell migration, fate determination, adhesion, and axon guidance. Avian models have, so far, enabled key insights into craniofacial and peripheral nervous system development. Yet, the molecular mechanisms driving trigeminal ganglion formation and subsequent nerve growth remain elusive. In this study, we performed RNA-sequencing at multiple stages of chick trigeminal ganglion development and generated a novel transcriptomic dataset that has been curated to illustrate temporally dynamic gene expression patterns. This publicly available resource identifies major pathways involved in trigeminal gangliogenesis, particularly with respect to the condensation and maturation of placode-derived neurons, thus inviting new lines of research into the essential processes governing trigeminal ganglion development.

2025-01-01 | GSE282770 | GEO

Transcriptomic Analysis of Trigeminal Ganglia and Spinal Trigeminal Nucleus Caudalis in Mice with Chronic Inflammatory Temporomandibular Joint Pain

Project description:Purpose: In this study, we aimed to analyze lncRNA expression in the whole transcriptome of trigeminal ganglia (TG) and spinal trigeminal nucleus caudalis (Sp5C) in a chronic inflammatory TMJ pain mouse model. Chronic inflammatory TMJ pain was induced by intra-TMJ injection of complete Freund's adjuvant (CFA). The lncRNA expression patterns in the whole transcriptome of TG and Sp5C were profiled with RNA sequencing.

2022-06-01 | GSE188922 | GEO

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

Effects of Nogo-A deletion on the trigeminal ganglion

Project description:Nogo-A is a major regulator of neural development and regeneration in the central nervous system, but its role in tooth innervation remains largely unknown. Neurons of the trigeminal ganglion innervate the teeth. We showed that Nogo-A is expressed in the trigeminal ganglion and tooth-related nerve fibres. Nogo-A deletion in mice leads to a less complex neuronal network when compared to wild-type animals. Bulk RNA sequencing on the trigeminal ganglia of Nogo-A KO and wild-type mice revealed gene expression changes associated with alterations in neurotrophin signalling and neuronal synaptic formation during the development and maturation of the trigeminal neurons.

2024-12-04 | GSE283391 | GEO

The star-nosed mole reveals clues to the molecular basis of mammalian touch.

Project description:Little is known about the molecular mechanisms underlying mammalian touch transduction. To identify novel candidate transducers, we examined the molecular and cellular basis of touch in one of the most sensitive tactile organs in the animal kingdom, the star of the star-nosed mole. Our findings demonstrate that the trigeminal ganglia innervating the star are enriched in tactile-sensitive neurons, resulting in a higher proportion of light touch fibers and lower proportion of nociceptors compared to the dorsal root ganglia innervating the rest of the body. We exploit this difference using transcriptome analysis of the star-nosed mole sensory ganglia to identify novel candidate mammalian touch and pain transducers. The most enriched candidates are also expressed in mouse somatosesensory ganglia, suggesting they may mediate transduction in diverse species and are not unique to moles. These findings highlight the utility of examining diverse and specialized species to address fundamental questions in mammalian biology. Examination of the transcriptome of 3 trigeminal and 3 dorsal root ganglia

2013-05-31 | E-GEOD-47480 | biostudies-arrayexpress

Transcription profiling of trigeminal ganglia of Brn3a knockout and wild type mice to determine the regulatory targets of transcription factor Brn3a.

Project description:Mice lacking the POU-domain transcription factor Brn3a exhibit marked defects in sensory axon growth and abnormal sensory apoptosis. We have determined the regulatory targets of Brn3a in the developing trigeminal ganglion using microarray analysis of Brn3a mutant mice. These results show that Brn3 mediates the coordinated expression of neurotransmitter systems, ion channels, structural components of axons and inter- and intracellular signaling systems. Loss of Brn3a also results in the ectopic expression of transcription factors normally detected in earlier developmental stages and in other areas of the nervous system. Target gene expression is normal in heterozygous mice, consistent with prior work showing that autoregulation by Brn3a results in gene dosage compensation. Detailed examination of the expression of several of these downstream genes reveals that the regulatory role of Brn3a in the trigeminal ganglion appears to be conserved in more posterior sensory ganglia but not in the CNS neurons that express this factor. Experiment Overall Design: Microarrays used to compare the patterns of gene expression in the trigeminal ganglia of Brn3a knockout and wild-type mice. Embryonic day 13.5 (E13.5) was chosen because at this point in development mutant mice exhibit major defects in sensory axon growth, but have yet to undergo the period of extensive sensory neuron death associated with later stages.

2007-11-01 | E-GEOD-3895 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data