Effects of Nogo-A deletion on the trigeminal ganglion
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ABSTRACT:
PROVIDER: PRJNA1193571 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31590014_1.fastq.gz | Fastqsanger.gz | |||
| SRR31590014_2.fastq.gz | Fastqsanger.gz | |||
| SRR31590015_1.fastq.gz | Fastqsanger.gz | |||
| SRR31590015_2.fastq.gz | Fastqsanger.gz | |||
| SRR31590016_1.fastq.gz | Fastqsanger.gz |
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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
Project description:Nogo-A is a major player in the regulation of neural development and regeneration, and it is the target of several clinical trials. Despite its high clinical relevance, the functions of Nogo-A outside the central nervous system are mostly unknown. In this work, we investigated the role of Nogo-A in tooth development in mouse transgenic models. We observed that Nogo-A is expressed in ameloblasts, the cells responsible for the formation of enamel. We show that the deletion of Nogo-A in the dental epithelium leads to the formation of defective enamel. By RNA sequencing we showed that this phenotype is associated with the overexpression of clusters of genes involved in cell differentiation and production of enamel.
2022-01-01 | GSE160829 | GEO
Project description:Trigeminal ganglion non-neuronal cells contain glial, endothelila, smooth muscle, immune cells and fibroblasts.
2023-12-07 | GSE240432 | GEO
Project description:Exosomes derived from rat trigeminal ganglion neurons (TGN) were harvested as control group. Exosomes derived from TGN after internalizing exosomes derived from stem cells from human exfoliated deciduous teeth (S-Exo) were harvested as treatment group.
2024-01-22 | PXD048746 |
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:RNA-seq: H3K9ac regulated by HDAC3 in trigeminal ganglion of SD rat trigeminal neuralgia model
| PRJEB46592 | ENA
Project description:Purpose: The cellular composition of the trigeminal ganglion is altered in the mouse model of 22q11.2 deletion syndrome (the LgDel mouse). The goal of this study is to use RNA-seq to identify transcriptional differences in the embryonic day 10.5 trigeminal ganglion that prefigure changes in mature cell identity in this cranial nerve ganglion. Methods: Trigeminal ganglion mRNA profiles of E10.5 trigeminal ganglia from WT and LgDel mice were generated by deep sequencing. Ganglia samples were prepared as pools of at least 6 ganglia each, from at least 3 embryos. 5 biological replicates of LgDel and WT pools were sequenced. Paired-end libraries were constructed according to the Illumina protocol for the HiSeq2000 platform. Each pooled CNgV RNA sample, defined as a single biological replicate, was fragmented prior to cDNA conversion to ensure transcript coverage. WT (n = 5 replicates) and LgDel (n = 5 replicates) were subjected to sequencing (~100 million paired-end reads/replicate, 100 bp read length) on the Illumina HiSeq2000 platform. Quality-filtered reads were aligned against the mouse reference genome (GRCm38/mm10) using HISAT2 (v.2.1.0). These alignments were indexed using SAMtools (v.1.4) and aligned reads assembled into transcripts using Cufflinks (v.2.2.1) (58). Differential expression analysis was performed using Cufflinks. Validation of key transcriptional differences was performed by SYBR Green qPCR. Results: For WT RNA-Seq, 111–123 million paired-end reads were generated after QC filtering, and 97.3–97.9% of the reads aligned to the mouse genome reference sequence. For LgDel RNA-Seq, 77–137 million paired-end reads were generated after QC filtering, and 94.3–97.8% of the reads aligned to the mouse genome reference sequence. LgDel versus wild-type (WT) CNgV transcriptomes differ significantly at E10.5 just after the ganglion has coalesced. Some changes parallel altered proportions of cranial placode versus cranial neural crest-derived CNgV cells. Others are consistent with a shift in anterior–posterior patterning associated with divergent LgDel cranial nerve differentiation. The most robust quantitative distinction, however, is statistically verifiable increased variability of expression levels for most of the over 17 000 genes expressed in common in LgDel versus WT CNgV. Conclusions: Quantitative expression changes of functionally relevant genes and increased stochastic variation across the entire CNgV transcriptome at the onset of CN V differentiation prefigure subsequent disruption of cranial nerve differentiation and oropharyngeal function in LgDel mice.
2021-04-27 | GSE173284 | GEO
Project description:Nogo, also called RTN4, functions through three isoforms including Nogo-A, -B, and -C. Although Nogo-A is a well-known CNS inhibitor and the level of Nogo-A is increased in muscles of ALS patients, its role in the regulation of skeletal muscle homeostasis and regeneration is still vague. In this study, we analyzed various pathological muscle condition of human and mouse model, and discovered significant increase of Nogo-A and myogenic factors. To understand the role of Nogo in skeletal muscle, muscle transcripts from Nogo+/+ and Nogo-/- mouse were analyzed and observed intensified gene expression involved in adipocyte differentiation and lipid metabolism, and reduced gene expression related to muscle differentiation and structure organization suggesting muscle disorder from muscle replacement with fat deposition. Skeletal muscle structure from Nogo null mice displayed dystrophic phenotypes including impaired myofiber structure and immune cell infiltrations, and dysregulated homeostatic features such as higher level of MyoD, procaspase 3, CHOP, and AKT compared to wild-type muscle. Notexin-injured Nogo deficient muscle resulted higher level of immune cell infiltration but defective in IL-6 production, a well-known myokine from immune cells, and abnormally upregulated regenerative muscle fibers than normal muscle. Therefore we hypothesized that increased Nogo-A in pathological conditions may regulate muscle regeneration. Then differentiating C2C12 cells and induced myogenic stem cells(iMSC) showed upregulated Nogo-A and Myogenin, and Nogo-A silencing in C2C12 cells abrogated the capability to differentiate into myotubes. In conclusion, Nogo functions to maintain muscle homeostasis and integrity, and altered Nogo-A expression in pathological muscle condition mediates muscle regeneration. These understanding suggests Nogo-A as a novel differentiation target for the treatment of myopathies at clinical set.
2019-05-31 | GSE131955 | GEO
Project description:Effects of Nogo-A deletion in the dental epithelium of the continuously growing mouse incisor
| PRJNA674603 | ENA
Project description:Nogo-A is a major player in neural development and regeneration, and it is the target of several clinical trials. However, its functions outside the nervous system are mostly unknown. We observed that Nogo-A is expressed in dental epithelial cells, responsible for the formation of enamel, and we showed that the deletion of Nogo-A in transgenic mouse models leads to the formation of defective enamel. We observed that Nogo-A directly interacts with molecules important for gene expression regulation, and its deletion perturbs their cellular localization. As a result, Nogo-A deletion induces overexpression of genes involved in cell differentiation and enamel production. Mechanistically, we demonstrated that intracellular Nogo-A, and not cell surface Nogo-A, is responsible for gene expression modulation. Taken together, our results indicate a new role for Nogo-A as regulator of enamel formation and suggest a new possible cell-autonomous function in regulating gene expression and cell differentiation.
2024-06-20 | PXD030386 | Pride