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Spinal cord of SOD1*G93A transgenic mice treated with PF-04457845 or vehicle

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE242942 | GEO | 2023/09/18

REPOSITORIES: GEO

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RNA-Seq result of Bulk spinal cord of SOD1*G93A transgenic mice treated with PF-04457845 or vehicle

Project description:SOD1*G93A transgenic mice were treated with PF-04457845 (a FAAH inhibitor)or vehicle . PF-04457845 extended survival of SOD1*G93A transgenic mice and resucued loss of motor neurons.

2023-09-18 | GSE242940 | GEO

Single cell RNA-Seq result of spinal cord of SOD1*G93A transgenic mice treated with PF-04457845 or vehicle

2023-09-18 | GSE242939 | GEO

Spinal cord of SOD1*G93A transgenic mice treated with PF-04457845 or vehicle

Project description:Spinal cord of SOD1*G93A transgenic mice treated with PF-04457845 or vehicle

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Preliminary Observation about Alteration of Proteins and Their Potential Functions in Spinal Cord of SOD1 G93A Transgenic Mice.

Project description:The protein abnormality participates in the development of ALS that meets with the widespread approval from major researchers. However, these currently found abnormal proteins aren't far enough to explain all pathogenesis of ALS. Therefore, the search of novel abnormal proteins participated in the pathogenesis of ALS is very necessary. In this study, we screened, compared and analyzed the differentially expressed proteins in the spinal cord of the SOD1 G93A transgenic and wild-type (WT) mice applying the isobaric tags for relative and absolute quantitation (iTRAQ) and the bioinformatics methods. The results revealed the details of significantly differentially expressed proteins between the SOD1 G93A transgenic and WT mice, and the damaged and/or regulated cellular components, molecular functions and biological processes and the significant enrichment pathways of these proteins. Our study comprehensively described the details of the possible abnormal proteins participated in the pathogenesis of SOD1 G93A transgenic mice, extensively explored their possible molecular mechanisms how to play the role in the development in this animal model, and provided some evidences and clues for further and deeply studying the relationship between the abnormal proteins and the pathogenesis of ALS in the other animal models and ALS patients.

| S-EPMC6097476 | biostudies-literature

RNA-Seq result of Bulk spinal cord of SOD1*G93A transgenic mice treated with PF-04457845 or vehicle

Project description:RNA-Seq result of Bulk spinal cord of SOD1*G93A transgenic mice treated with PF-04457845 or vehicle

| PRJNA1015587 | ENA

Single cell RNA-Seq result of spinal cord of SOD1*G93A transgenic mice treated with PF-04457845 or vehicle

Project description:Single cell RNA-Seq result of spinal cord of SOD1*G93A transgenic mice treated with PF-04457845 or vehicle

| PRJNA1015585 | ENA

Muscle Expression of SOD1(G93A) Modulates microRNA and mRNA Transcription Pattern Associated with the Myelination Process in the Spinal Cord of Transgenic Mice.

Project description:A crucial system severely affected in several neuromuscular diseases is the loss of effective connection between muscle and nerve, leading to a pathological non-communication between the two tissues. One of the best examples of impaired interplay between muscle and nerve is Amyotrophic Lateral Sclerosis, a neurodegenerative disease characterized by degeneration of motor neurons and muscle atrophy. Increasing evidences suggest that damage to motor neurons is enhanced by alterations in the neighboring non-neuronal cells and indicate that altered skeletal muscle might be the source of signals that impinge motor neuron activity and survival. Here we investigated whether muscle selective expression of SOD1(G93A) mutant gene modulates mRNAs and miRNAs expression at the level of spinal cord of MLC/SOD1(G93A) mice. Using a Taqman array, the Affymetrix Mouse Gene 2.0 ST approach and the MiRwalk 2.0 database, which provides information on miRNA and their predicted target genes, we revealed that muscle specific expression of SOD1(G93A) modulates relevant molecules of the genetic and epigenetic circuitry of myelin homeostasis in spinal cord of transgenic mice. Our study provides insights into the pathophysiological interplay between muscle and nerve and supports the hypothesis that muscle is a source of signals that can either positively or negatively affect the nervous system.

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Genetic biomarkers for ALS disease in transgenic SOD1(G93A) mice.

Project description:The pathophysiological mechanisms of both familial and sporadic Amyotrophic Lateral Sclerosis (ALS) are unknown, although growing evidence suggests that skeletal muscle tissue is a primary target of ALS toxicity. Skeletal muscle biopsies were performed on transgenic SOD1(G93A) mice, a mouse model of ALS, to determine genetic biomarkers of disease longevity. Mice were anesthetized with isoflurane, and three biopsy samples were obtained per animal at the three main stages of the disease. Transcriptional expression levels of seventeen genes, Ankrd1, Calm1, Col19a1, Fbxo32, Gsr, Impa1, Mef2c, Mt2, Myf5, Myod1, Myog, Nnt, Nogo A, Pax7, Rrad, Sln and Snx10, were tested in each muscle biopsy sample. Total RNA was extracted using TRIzol Reagent according to the manufacturer's protocol, and variations in gene expression were assayed by real-time PCR for all of the samples. The Pearson correlation coefficient was used to determine the linear correlation between transcriptional expression levels throughout disease progression and longevity. Consistent with the results obtained from total skeletal muscle of transgenic SOD1(G93A) mice and 74-day-old denervated mice, five genes (Mef2c, Gsr, Col19a1, Calm1 and Snx10) could be considered potential genetic biomarkers of longevity in transgenic SOD1(G93A) mice. These results are important because they may lead to the exploration of previously unexamined tissues in the search for new disease biomarkers and even to the application of these findings in human studies.

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Neuronal-glial communication perturbations in murine SOD1<sup>G93A</sup> spinal cord.

Project description:Amyotrophic lateral sclerosis (ALS) is an incurable disease characterized by proteinaceous aggregate accumulation and neuroinflammation culminating in rapidly progressive lower and upper motor neuron death. To interrogate cell-intrinsic and inter-cell type perturbations in ALS, single-nucleus RNA sequencing was performed on the lumbar spinal cord in the murine ALS model SOD1G93A transgenic and littermate control mice at peri-symptomatic onset stage of disease, age 90 days. This work uncovered perturbed tripartite synapse functions, complement activation and metabolic stress in the affected spinal cord; processes evidenced by cell death and proteolytic stress-associated gene sets. Concomitantly, these pro-damage events in the spinal cord co-existed with dysregulated reparative mechanisms. This work provides a resource of cell-specific niches in the ALS spinal cord and asserts that interwoven dysfunctional neuronal-glial communications mediating neurodegeneration are underway prior to overt disease manifestation and are recapitulated, in part, in the human post-mortem ALS spinal cord.

| S-EPMC8885678 | biostudies-literature

Expression data from mutant SOD1(G93A) transgenic mice

Project description:Expression profiling of spinal cord from SOD1(G93A) mice and age matched controls at ages 28, 42, 56, 70,98,112, and 126 days of age. We used microarrays to determine differential gene expression throughout disease progression in the spinal cord of mutant SOD1(G93A) model of ALS.

2009-10-17 | GSE18597 | GEO

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