Migraine RNA-seq
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB40032 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4796180.fastq.gz | Fastqsanger.gz | |||
| ERR4796190.fastq.gz | Fastqsanger.gz | |||
| ERR4796200.fastq.gz | Fastqsanger.gz | |||
| ERR4796210.fastq.gz | Fastqsanger.gz | |||
| ERR4796171.fastq.gz | Fastqsanger.gz |
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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
Project description:The persistent headaches characteristic of chronic migraine may stem from the activation and sensitization of primary afferent neurons within the trigeminovascular pathway. The molecular basis for this pathophysiology, however, remains incompletely understood. In this study, we demonstrated that SETDB2, a histone methyltransferase expressed in trigeminal ganglion (TG) neurons, plays a pivotal role in facilitating migraine-associated pain behaviors. We modelled chronic headache with repeated administration of nitroglycerin (NTG, a well-recognized migraine trigger in migraineurs) and observed a notable upregulation of SETDB2 in mouse TG neurons following NTG treatment. A comparable increase was also identified in the cerebrospinal fluid of migraine sufferers. Reversing the NTG-induced SETDB2 upregulation abrogated the increased trimethylation of histone H3K9 (H3K9me3) and alleviated established migraine-associated pain behaviors. Conversely, mimicking the upregulation of SETDB2 in intact TG neurons was sufficient to induce pain hypersensitivity. Moreover, we found that SETDB2 upregulation induced by NTG prevented the binding of the transcription factor KLF4 to the promoter of the insulin-degrading enzyme (Ide) gene. This, in turn, inhibited IDE expression, and hindered the degradation of calcitonin- gene-related peptide (CGRP), a promising target for preventing migraine, in TG neurons. Targeting the sensory SETDB2-KLF4-IDE transcriptional axis may present novel therapeutic opportunities for treating migraine.
2026-02-28 | GSE308023 | GEO
Project description:The persistent headaches characteristic of chronic migraine may stem from the activation and sensitization of primary afferent neurons within the trigeminovascular pathway. The molecular basis for this pathophysiology, however, remains incompletely understood. In this study, we demonstrated that SETDB2, a histone methyltransferase expressed in trigeminal ganglion (TG) neurons, plays a pivotal role in facilitating migraine-associated pain behaviors. We modelled chronic headache with repeated administration of nitroglycerin (NTG, a well-recognized migraine trigger in migraineurs) and observed a notable upregulation of SETDB2 in mouse TG neurons following NTG treatment. A comparable increase was also identified in the cerebrospinal fluid of migraine sufferers. Reversing the NTG-induced SETDB2 upregulation abrogated the increased trimethylation of histone H3K9 (H3K9me3) and alleviated established migraine-associated pain behaviors. Conversely, mimicking the upregulation of SETDB2 in intact TG neurons was sufficient to induce pain hypersensitivity. Moreover, we found that SETDB2 upregulation induced by NTG prevented the binding of the transcription factor KLF4 to the promoter of the insulin-degrading enzyme (Ide) gene. This, in turn, inhibited IDE expression, and hindered the degradation of calcitonin- gene-related peptide (CGRP), a promising target for preventing migraine, in TG neurons. Targeting the sensory SETDB2-KLF4-IDE transcriptional axis may present novel therapeutic opportunities for treating migraine.
2026-02-28 | GSE308024 | GEO
Project description:DNA methylation in episodic migraine and medication overuse headache.
| PRJNA1416851 | ENA
Project description:Disease- and headache-Specific miRNA signatures and predicted targets in the peripheral blood mononuclear cells of migraineurs
| PRJEB46142 | ENA
Project description:Background: Migraine is a prevalent neurological disorder that affects a significant portion of the global population. Previous studies have suggested that microRNAs (miRNAs) may play a crucial role in the pathogenesis of migraine. This study aims to explore the potential functions of miRNAs through sequencing analysis of the Sp5C in a migraine mouse model. Method: Migraine mouse models were established through repeated inflammatory soup dural injections. Total RNA was extracted from the Sp5C of both the migraine and control groups. High-throughput sequencing technology was employed to analyze the miRNA expression profiles, followed by differential expression analysis using bioinformatics tools. Pathway enrichment analysis was performed based on differential expressed miRNAs, and literature review was conducted to identify target genes for subsequent animal experiments. Results: Compared to the control group, we identified four miRNAs with differential expression (fold change ≥1.5, P < 0.05), all of which were upregulated in the migraine model group. These miRNAs included miR-12179-5p, miR-23b-5p, miR-214-5p, and miR-6239. We employed online miRNA prediction tools (Targetscan, miRWalk, and miRDB) and obtained 7,909 predicted target genes. Bioinformatics analysis of these target genes identified several enriched signaling pathways, with particular interest in chemotaxis, immune receptor activity, immune system development, and the MAPK signaling pathway. These pathways play important roles in mediating pain and neuroinflammation. Based on a literature review and bioinformatics analysis, we identified Cxcr5 as a potential key gene for further research. Conclusion: Our results indicated that four upregulated miRNAs (miR-12179-5p, miR-23b-5p, miR-214-5p, and miR-6239) were identified in the migraine model compared to the control group. Whether Cxcr5 can serve as a key regulatory gene for migraine treatment requires further experimental validation.
2026-02-11 | GSE281596 | GEO
Project description:Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (âFHM1 R192Q miceâ) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine. Cortical RNA expression analysis using deepSAGE sequencing of wild-type (C57BL/6J) or transgenic R192Q FHM1 mice (n=6 per experimental group) 24 hours after sham surgery or the induction of 7 cortical spreading depression episodes
2016-04-14 | E-GEOD-67933 | biostudies-arrayexpress
Project description:Background：CircRNAs are non-coding RNA molecules that have recently been described and shown to regulate miRNA functionality. While recent studies have suggested such circRNAs to be associated with pain related diseases in humans, no comprehensive migraine-related circRNA profiles have been generated and there is currently no clear understanding of whether they can serve as regulators of migraine pathology. Methods:We initially conducted a circRNA microarray analysis of the plasma of migraine patients and healthy controls. Based upon these data, we then selected 8 differentially expressed circRNAs and confirmed their expression in more migraine patient plasma samples via real-time PCR. We then performed functional and pathway enrichment analyses. Lastly, using a robust rank aggregation approach, we constructed a ceRNA network according to predicted circRNA–miRNA and miRNA–mRNA pairs in these migraine patient samples. Results:we were able to detect 2039 circRNAs in our patient samples, with and 794 of 1245 these circRNAs being up- and down-regulated in migraine patients relative to controls, respectively (fold change ≥1.5, P < 0.01). A qRT-PCR analysis confirmed that the expression of hsa_circRNA_100236, hsa_circRNA_102413, and hsa_circRNA_000367 was significantly enhanced in migraine patients, whereas the expression of hsa_circRNA_103809, hsa_circRNA_103670, and hsa_circRNA_101833 was significantly reduced in these individuals relative to healthy controls. We found these differentially regulated circRNAs to be associated with numerous predicted biological processes, with enrichment analyses suggesting that they may modulate PI3K-Akt signaling so as to promote inflammation to drive migraine development. However, further research will be needed to formally test these mechanistic possibilities and to validate these circRNAs as potential biomarkers of migraine patients.Conclusions: our results offer new potential insights into the mechanistic basis of this condition, and suggest that hsa_circRNA_000367 and hsa_circRNA_102413 may offer value as regulators of migraine pathology.
2020-09-05 | GSE157495 | GEO
Project description:Familial Hemiplegic Migraine type 1 (FHM1) is a rare monogenic subtype of migraine with aura caused by mutations in CACNA1A that encodes the a1A subunit of voltage-gated CaV2.1 calcium channels. Transgenic knock-in mice that carry the human FHM1 R192Q missense mutation (“FHM1 R192Q mice”) exhibit an increased susceptibility to cortical spreading depression (CSD), the mechanism underlying migraine aura. Here we analysed gene expression profiles from isolated cortical tissue of FHM1 R192Q mice 24 hours after experimentally induced CSD in order to identify molecular pathways affected by CSD. Gene expression profiles were generated using deep Serial Analysis of Gene Expression sequencing. Our data reveal a signature of inflammatory signalling upon CSD in the cortex of both mutant and wild-type mice. However, only in the brains of FHM1 R192Q mice specific genes are up-regulated in response to CSD that are implicated in interferon-related inflammatory signalling. Our findings show that CSD modulates inflammatory processes in both wild-type and mutant brains, but that an additional unique inflammatory signature becomes expressed after CSD in a relevant mouse model of migraine.
2016-04-14 | GSE67933 | GEO
Project description:A comprehensive bulk RNA-Seq analysis with two distinct time points was undertaken, comprising a cohort of 22 individuals affected by interictal migraine and a comparative group of 30 individuals in robust health. It is noteworthy that both cohorts were entirely free from any headache manifestations and did not utilize either acute or chronic medication. The subsequent investigation entailed a rigorous examination of the interictal migraineurs in relation to the healthy control cohort, with meticulous attention given to the identification and validation of replicable findings.
2024-09-12 | E-MTAB-13397 | biostudies-arrayexpress