Migraine RNA-seq
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB40032 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Colorectal cancer (CRC) is the third most common cancer and the fourth leading cause of cancer-related death in the world. Despite potentially curative surgery and the use of modern adjuvant chemotherapy, up to 40% of CRC patients subsequently develop local tumor relapse or metastatic disease. Currently, aside from post-operative pathological staging, early follow up of the patients does not include a specific test or any other evaluation that could predict disease recurrence. Therefore, exploring and identifying novel biomarkers of CRC’s following diagnosis of the primary tumor may help us in identifying patients at high risk for recurrence.
Modifications in signaling pathways and their regulation by microRNAs (miRNAs) are being evaluated as biomarkers and therapeutic targets for cancer in general and CRC in particular. It has been established, although not completely, that miRNAs have a role in initiation and progression of CRC. Modifications of miRNAs have been recorded in CRC tumors, and the expression patterns of these miRNAs could in principle biomark this cancer’s phenotype. As miRNAs are well documented to regulate critical molecules in signaling pathways, their regulation of tumor relevant pathways may also serve to further sub-classify patients into drug responsive groups. Moreover, miRNAs may be sampled from peripheral blood and are available as a non-invasive diagnostic method, their application as biomarkers is of special interest.
In this study the investigators aim to quantify miRNA levels in human colon and rectal tumors, tumor adjacent and normal tissues. By comparing this data from a large cohort of patients, the investigators aim to identify specific, relevant miRNAs that may serve as biomarkers to stratify CRC patients according to their clinical characteristics such as disease stage, specific treatment, prognosis and disease recurrence.
| 2134048 | ecrin-mdr-crc
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:Blood genomic profiling has been applied to disorders of the blood and various organ systems including brain to elucidate disease mechanisms and identify surrogate disease markers. Since most studies have not examined specific cell types, we performed a preliminary genomic survey of major blood cell types from normal individuals using microarrays. CD4+ T cells, CD8+ T cells, CD19+ B cells, CD56+ natural killer cells, and CD14+ monocytes were negatively selected using the RosetteSep antibody cocktail, while polymorphonuclear leukocytes were separated with density gradient media. Genes differentially expressed by each cell type were identified. To demonstrate the potential use of such cell subtype-specific genomic expression data, a number of the major genes previously reported to be regulated in ischemic stroke, migraine, and Tourette syndrome are shown to be associated with distinct cell populations in blood. These specific gene expression, cell-type-related profiles will need to be confirmed in larger data sets and could be used to study these and many other neurological diseases.
2015-09-03 | GSE72642 | GEO
Project description:Blood genomic profiling has been applied to disorders of the blood and various organ systems including brain to elucidate disease mechanisms and identify surrogate disease markers. Since most studies have not examined specific cell types, we performed a preliminary genomic survey of major blood cell types from normal individuals using microarrays. CD4+ T cells, CD8+ T cells, CD19+ B cells, CD56+ natural killer cells, and CD14+ monocytes were negatively selected using the RosetteSep antibody cocktail, while polymorphonuclear leukocytes were separated with density gradient media. Genes differentially expressed by each cell type were identified. To demonstrate the potential use of such cell subtype-specific genomic expression data, a number of the major genes previously reported to be regulated in ischemic stroke, migraine, and Tourette syndrome are shown to be associated with distinct cell populations in blood. These specific gene expression, cell-type-related profiles will need to be confirmed in larger data sets and could be used to study these and many other neurological diseases. This study includes data from major blood cell types from normal individuals. These cell types include CD4+ T cells, CD8+ T cells, CD19+ B cells, CD56+ natural killer cells, CD14+ monocytes and PMN (polymorphonuclear cells). The data were hybridized on 3 separate batches of gene chips.
2015-09-03 | E-GEOD-72642 | biostudies-arrayexpress
Project description:Research purpose: To explore the key targets and core signal pathways of XHT (Xinhuitong, XHT) in regulating coronary heart disease with Qi deficiency and blood stasis syndrome through transcriptomics, and reveal the transcriptional regulatory network of XHT in treating coronary heart disease with Qi deficiency and blood stasis syndrome. Research method: Using transcriptomics RNA-Seq technology, gene sequencing of myocardial tissues in the ischemic marginal zone of the Qi deficiency and blood stasis syndrome model group and the high-dose Yiqi Huoxue prescription group and searching for differential genes, from the perspective of gene regulation and expression patterns To study the possible effective drug targets and effect mechanism pathways of XHT in the treatment of coronary heart disease with Qi deficiency and blood stasis syndrome, and to further explore the treatment of coronary heart disease with Qi deficiency and blood by Chinese medicine compound prescriptions. The possible pharmacological mechanism of blood stasis syndrome, and the key molecular nodes and effect mechanism pathways suggested by it are verified by molecular biology methods.
2023-02-13 | GSE211248 | GEO
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:Migraine is primarily mediated via CGRP signaling on various tissues to induce pain and other migraine symptoms. We characterize the role of migraine related CGRP signaling on meningeal lymphatic vessels from mouse meningeal lymphatic tissue. In this dataset, we include the expression data obtained from lyve-1 positive meningeal lymphatic endothelial cells from Lyve-1 cre mediated HA-tagged ribosomes from mice with the NTG mediated model of migraine. These data are used to obtain 700 genes that are differentially expressed in meningeal lymphatic tissue in response to NTG induced migraine.
2024-05-08 | GSE266558 | GEO
Project description:Although several underlying pathophysiological processes have been explored, the origin and precise pathomechanism of migraine are still being debated. Inflammatory pathways have been suggested to play role in migraine, trigeminal nociceptor sensitisation, thereby causing hyperalgesia and allodynia. The aim of the present study was to investigate gene expression changes in trigeminal ganglia (TRG), central trigeminal nucleus caudalis (TNC) and peripheral blood mononuclear cells (PBMC) evoked by Complete Freund’s Adjuvant (CFA) induced peripheral inflammation. 512 differentially expressed genes were found between CFA-treated and contralateral TRG samples 7 days after CFA injection. The mRNA expression changes of G-protein coupled receptor 39 (Gpr39), kisspeptin-1 receptor (Kiss1r), kisspeptin (Kiss1) and Lkaaear1 were selected for validation. They were most upregulated on day 3 in TRGs of the CFA-treated side. CFA-induced significant orofacial mechanical allodynia in one day with a maximum on day 3. This correlated with patterns of neuronal (Fosb), glial (Iba1), and astrocyte (Gfap) activation markers in both TRG and TNC, and surprisingly in PBMCs. Similar transcriptional changes of Cgrp, the well-known key molecule in migraine pathophysiology, were also revealed. In TNCs, gene expression changes similar to TRGs were observed but Kiss1r transcripts were not significantly altered while Neurod2 was observed only in TNC. These results could indicate the involvement of Gpr39, Kiss1r and synaptic plasticity associated Lkaaear1, Neurod2 genes in the cascade of events resulting in the sensitization underlying migraine headache and the accompanying facial allodynia.
2018-12-14 | GSE111160 | GEO
Project description:By analyse the tissue/blood variant spectrum model using NGS, the present clinical trial aims to elucidate the genetic basis of CRC in Chinese; to establish of CRC genetic map in Chinese patients; to identification new genetic biomarkers, drug and pathways; and to subtyping for precision treatment and management for Chinese CRC patients.
| 2326961 | ecrin-mdr-crc