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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE242939 | 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

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. Samples were collected from male B6SJL SOD1(G93A) and age matched controls. 3 samples were collected representing each genotype and age group for RNA extraction and hybridization on Affymetrix microarrays.

2009-10-17 | E-GEOD-18597 | biostudies-arrayexpress

Profiling wt SOD versus ALS SOD1(G93A) mutant

Project description:Whole-genome profiling of SH-SY5Y cells was done on neuroblastoma SH-SY5Y stably transfected with cDNAs coding for SOD1WT or the mutant SOD1(G93A) protein.

2010-12-22 | GSE21298 | GEO

CNS-derived extracellular vesicles from superoxide dismutase 1 (SOD1)G93A ALS mice originate from astrocytes and neurons and carry misfolded SOD1

Project description:Extracellular vesicles (EVs) are secreted by myriad cells in culture and also by unicellular organisms, and their identification in mammalian fluids suggests that EV release also occurs at the organism level. However, although it is clearly important to better understand EVs' roles in organismal biology, EVs in solid tissues have received little attention. Here, we modified a protocol for EV isolation from primary neural cell culture to collect EVs from frozen whole murine and human neural tissues by serial centrifugation and purification on a sucrose gradient. Quantitative proteomics comparing brain-derived EVs from nontransgenic (NTg) and a transgenic amyotrophic lateral sclerosis (ALS) mouse model, superoxide dismutase 1 (SOD1) G93A , revealed that these EVs contain canonical exosomal markers and are enriched in synaptic and RNA-binding proteins. The compiled brain EV proteome contained numerous proteins implicated in ALS, and EVs from SOD1 G93A mice were significantly depleted in myelin-oligodendrocyte glycoprotein compared with those from NTg animals. We observed that brain- and spinal cord–derived EVs, from NTg and SOD1 G93A mice, are positive for the astrocyte marker GLAST and the synaptic marker SNAP25, whereas CD11b, a microglial marker, was largely absent. EVs from brains and spinal cords of the SOD1 G93A ALS mouse model, as well as from human SOD1 familial ALS patient spinal cord, contained abundant misfolded and nonnative disulfide-cross-linked aggregated SOD1. Our results indicate that CNS-derived EVs from an ALS animal model contain pathogenic disease-causing proteins and suggest that brain astrocytes and neurons, but not microglia, are the main EV source.

2020-09-11 | PXD021396 | Pride

miRNA expression in fast and slow skeletal muscle of wild type and SOD1-G93A mice

Project description:Amyotrophic lateral sclerosis (ALS) is a lethal motor neuron disease that progressively debilitates neuronal cells that control voluntary muscle activity. In a mouse model of ALS that expresses mutated human superoxide dismutase 1 (SOD1-G93A) skeletal muscle is one of the tissues affected early by mutant SOD1 toxicity. Fast-twitch and slow-twitch muscles are differentially affected in ALS patients and in the SOD1-G93A model, fast-twitch muscles being more vulnerable. We used miRNA microarrays to investigate miRNA alterations in fast-twitch (EDL) and slow-twitch (soleus) skeletal muscles of symptomatic SOD1-G93A animals and their age-matched wild type littermates.

2014-03-04 | GSE55507 | GEO

scRNAseq from spinal cords of SOD1-G93A and WT mice

Project description:We prepared spinal cords from SOD1-G93A and WT mice treated with vehicle or the RIPK1 inhibitor Nec-1s, which were single cell RNA sequenced using the DropSeq protocol.

2021-03-24 | GSE167198 | GEO

Gene expression profile of G93A-SOD1 mouse spinal cord, blood and muscle

Project description:To investigate the usefulness of gene expression as diagnostic biomarkers, we compared whole genome expression profiles of lumbar spinal cord with profiles of peripheral blood and tibialis anterior muscle in 16 mutant G93A-SOD1 mice and 15 wild type littermates. Total RNA obtained from blood, tibialis anterior muscle and lumbar spinal cord of G93A-SOD1 mice compared to wild type littermates.

2013-03-01 | E-GEOD-27933 | biostudies-arrayexpress

miRNA expression in fast and slow skeletal muscle of wild type and SOD1-G93A mice

2014-03-04 | E-GEOD-55507 | biostudies-arrayexpress

Profiling wt SOD versus ALS SOD1(G93A) mutant

Project description:Whole-genome profiling of SH-SY5Y cells was done on neuroblastoma SH-SY5Y stably transfected with cDNAs coding for SOD1WT or the mutant SOD1(G93A) protein. Five wt SOD versus five mutant SOD

2010-12-22 | E-GEOD-21298 | biostudies-arrayexpress

Analysis of expression in SOD1 transgenic mouse spinal cord

Project description:mRNA expression in the spinal cords of the G93A-SOD1 familial ALS transgenic mouse model was compared to that in nontransgenic (Normal mouse) and transgenic mice expressing wild-type (WT)SOD1. Gene Ontology (GO)analysis was used to characterize differences in expression between G93A-SOD1 mouse and nontransgenic mouse spinal cord. Changes in multiple GO categories were found. Many of these were associated with subsystems involving cell-cell communication and intracellular signal transduction. Expression profiles of mice expressing WT-SOD1 did not differ from nontransgenic mice. In contrast, protein profiling using proteomics technology indicated changes in mitochondrial protein expression in the G93A-SOD1 mouse spinal cord that were not found in the mRNA expression analysis. Keywords: Disease state analysis, time course, transgenic mice

2006-03-09 | GSE4390 | GEO

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