Ontology highlight
ABSTRACT:
PROVIDER: PRJNA577447 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cerebral palsy is caused be an upper motor neuron lesion which casues spasticity as well as secondary effects on muscle . Muscle from cerebral palsy patients is has been shown to be smaller, with more ECM and longer sarcomere lengths; We used microarrays to globally investigate the transcriptional adaptations of cerebral palsy muscle and research which muscle pathways are altered in the diseased state Experiment Overall Design: Muscle biopsies were taken from children undergoing surgery which exposed wrist muscle extensors (n=8) and flexors (n=8) in both cerebral palsy patients (n=6) and control patients (n=2) for RNA extraction and hybridization to Affymetrix GeneChips . Cerebral palsy patients were classified by a number of clinical scores.
2009-09-05 | E-GEOD-11686 | biostudies-arrayexpress
Project description:Cerebral palsy is primarily an upper motor neuron disease that results in a spectrum of progressive movement disorders. Secondary to the neurological lesion, muscles from patients with cerebral palsy are often spastic and form debilitating contractures that limit range of motion and joint function. With no genetic component, the pathology of skeletal muscle in cerebral palsy is a response to aberrant neurological input in ways that are not fully understood. This study was designed to gain further understanding of the skeletal muscle response to cerebral palsy using microarrays and correlating the transcriptional data with functional measures. Hamstring biopsies from gracilis and semitendinosus muscles were obtained from a cohort of patients with cerebral palsy (n=10) and typically developing patients (n=10) undergoing surgery. Affymetrix HG-U133A 2.0 chips (n=40) were used and expression data was verified for 6 transcripts using quantitative real-time PCR, as well as for two genes not on the microarray. Chips were clustered based on their expression and those from patients with cerebral palsy clustered separately. Significant genes were determined conservatively based on the overlap of three summarization algorithms (n=1,398). Significantly altered genes were analyzed for over-representation among gene ontologies, transcription factors, pathways, microRNA and muscle specific networks. These results centered on an increase in extracellular matrix expression in cerebral palsy as well as a decrease in metabolism and ubiquitin ligase activity. The increase in extracellular matrix products was correlated with mechanical measures demonstrating the importance in disability. These data lay a framework for further studies and novel therapies. Skeletal muscle biopsies from both the gracilis and semitendinosus were obtained during surgery for 20 pediatric subjects for affymetrix microarray analysis. We obtained a group of 10 patients undergoing medial hamstring lengthening in the cerebral palsy group and 10 patients undergoing ACL reconstruction with hamstring autograft in the control group. This provided 40 microarrays in 4 groups to analyze the effect of cerebral palsy and also differences between muscles.
2012-11-21 | E-GEOD-31243 | biostudies-arrayexpress
Project description:Cerebral palsy is caused be an upper motor neuron lesion which casues spasticity as well as secondary effects on muscle . Muscle from cerebral palsy patients is has been shown to be smaller, with more ECM and longer sarcomere lengths We used microarrays to globally investigate the transcriptional adaptations of cerebral palsy muscle and research which muscle pathways are altered in the diseased state Keywords: Disease state analysis
2009-08-26 | GSE11686 | GEO
Project description:Cerebral palsy is primarily an upper motor neuron disease that results in a spectrum of progressive movement disorders. Secondary to the neurological lesion, muscles from patients with cerebral palsy are often spastic and form debilitating contractures that limit range of motion and joint function. With no genetic component, the pathology of skeletal muscle in cerebral palsy is a response to aberrant neurological input in ways that are not fully understood. This study was designed to gain further understanding of the skeletal muscle response to cerebral palsy using microarrays and correlating the transcriptional data with functional measures. Hamstring biopsies from gracilis and semitendinosus muscles were obtained from a cohort of patients with cerebral palsy (n=10) and typically developing patients (n=10) undergoing surgery. Affymetrix HG-U133A 2.0 chips (n=40) were used and expression data was verified for 6 transcripts using quantitative real-time PCR, as well as for two genes not on the microarray. Chips were clustered based on their expression and those from patients with cerebral palsy clustered separately. Significant genes were determined conservatively based on the overlap of three summarization algorithms (n=1,398). Significantly altered genes were analyzed for over-representation among gene ontologies, transcription factors, pathways, microRNA and muscle specific networks. These results centered on an increase in extracellular matrix expression in cerebral palsy as well as a decrease in metabolism and ubiquitin ligase activity. The increase in extracellular matrix products was correlated with mechanical measures demonstrating the importance in disability. These data lay a framework for further studies and novel therapies.
2012-11-21 | GSE31243 | GEO
Project description:Our results revealed that hypoxic-ischemic brain injury decreased the overall 5hmC abundance in rat temporal cortex, and these results suggest that 5hmC modifications are involved in the cerebral palsy pathogenesis.
2019-07-04 | GSE133787 | GEO
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
Project description:WGS Cram files from the Childhood Cerebral Palsy Integrated Neuroscience Discovery Network "CP-NET" - Clinical Database Platforms - Phase 3 project.
| EGAD00001010014 | EGA
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:In this study, the properties of circulating EVs were examined in cerebral palsy (CP) and typically developed (TD) individuals at rest and after aerobic exercise. We performed smallRNA-seq anf focused on the microRNA cargo of EVs
2022-12-10 | GSE218103 | GEO