GM604 regulates developmental neurogenesis pathways and the expression of genes associated with amyotrophic lateral sclerosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA471631 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7170040.fastq.gz | Fastqsanger.gz | |||
| SRR7170050.fastq.gz | Fastqsanger.gz | |||
| SRR7170060.fastq.gz | Fastqsanger.gz | |||
| SRR7170041.fastq.gz | Fastqsanger.gz | |||
| SRR7170051.fastq.gz | Fastqsanger.gz |
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Project description:Identification of familial amyotrophic lateral sclerosis (fALS) related genes. Material from three hSOD1(G93A) transgenic mice was compared to material from three non-transgenic control mice using an alternating loop design on two-colour cDNA microarrays. Statistical data management and analysis: postgreSQL relational database (www.postgresql.org), Perl, and R (www.r-project.org); pin-wise lowess-regression based normalisation (Yang et al., 2002 [PMID: 11842121]); mixed ANOVA-model. Keywords = amyotrophic lateral sclerosis, ALS, SOD1 mouse model
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Project description:This study was designed to identify gene expression changes in skeletal muscle that could define reliably the degree of the severity of Amyotrophic lateral sclerosis (ALS). All samples were from human biopsies, either from healthy muscles or from muscle whose patients were clearly diagnosed as having Amyotrophic Lateral Sclerosis (ALS)
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Project description:Spatiotemporal dynamics of molecular pathology in amyotrophic lateral sclerosis
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Project description:Background: Amyotrophic lateral sclerosis (ALS) is currently an incurable disease without highly effective pharmacological treatments. The peptide drug GM604 (GM6) was developed as a candidate ALS therapy, which has demonstrated safety and encouraging outcomes in a phase II clinical trial. GM6 is hypothesized to bolster neuron survival through regulation of developmental pathways, but mechanisms of action are not fully understood. Methods: This study used RNA-seq to evaluate transcriptome responses in SH-SY5Y neuroblastoma cells following GM6 treatment (6, 24 and 48 hours). Results: We identified 2867 protein-coding genes with expression significantly altered by GM6 (FDR < 0.10). Early (6 hour) responses included up-regulation of Notch and hedgehog signaling components, with increased expression of developmental genes mediating neurogenesis and axon growth. Prolonged GM6 treatment (24 and 48 hours) altered the expression of genes contributing to cell adhesion and the extracellular matrix. GM6 further down-regulated the expression of genes associated with mitochondria, inflammatory responses, mRNA processing and chromatin organization. GM6-increased genes were located near GC-rich motifs interacting with C2H2 zinc finger transcription factors, whereas GM6-decreased genes were located near AT-rich motifs associated with helix-turn-helix homeodomain factors. Such motifs interacted with a diverse network of transcription factors encoded by GM6-regulated genes (STAT3, HOXD11, HES7, GLI1). We identified 77 ALS-associated genes with expression significantly altered by GM6 treatment (FDR < 0.10), which were known to function in neurogenesis, axon guidance and the intrinsic apoptosis pathway. Discussion: Our findings support the hypothesis that GM6 acts through developmental-stage pathways to influence neuron survival. Gene expression responses were consistent with neurotrophic effects, ECM modulation, and activation of the Notch and hedgehog neurodevelopmental pathways. This multifaceted mechanism of action is unique among existing ALS drug candidates and may be applicable to multiple neurodegenerative diseases.
2018-10-24 | GSE114510 | GEO
Project description:Importance: Amyotrophic lateral sclerosis demonstrated changes in peripheral immune cells and proteins. However, the relationship between comprehensive immune profiles and clinical progression remained unclear. Objective: To identify the immune cells and proteins related to amyotrophic lateral sclerosis progression rate. Design: This case-control study enrolled healthy volunteers and patients with amyotrophic lateral sclerosis from March 29, 2021, to October 31, 2022. Setting: Tokushima University Hospital and Takeda Pharmaceutical Company Limited in Japan. Participants: This study screened 46 subjects to enroll 30 patients with amyotrophic lateral sclerosis within 2 years from onset and 10 healthy volunteers. Patients with rapid and non-rapid amyotrophic lateral sclerosis were those with Revised Amyotrophic Lateral Sclerosis Functional Rating Scale decreases of ≥1.0/month and <1.0/month, respectively. Exposure(s): Peripheral blood samples were collected. Main Outcome(s) and Measure(s): The progression rate as assessed with the Revised Amyotrophic Lateral Sclerosis Functional Rating Scale decrease/month and the immune cell and protein profiles via single-cell RNA sequencing and immunoproteomics. Results: Samples of 7 (mean [standard deviation] age: 69.8 [14.4] years; male, 3) and 23 (60.7 [10.8] years; male, 17) patients with rapid and non-rapid amyotrophic lateral sclerosis, respectively, and 10 healthy volunteers (63.6 [10.2] years; male, 7) were analyzed. The ratios of T helper 17/regulatory T cells, mature/naïve CD8 T cells, and mature/naïve natural killer cells were significantly higher in rapid than in non-rapid amyotrophic lateral sclerosis. The ratio of T helper 17/regulatory T cells was significantly correlated with the progression rate. The immunoproteomics identified killer cell lectin-like receptor D1, trefoil factor 2, keratin 19, interleukin-17A, YTH N6-methyladenosine RNA binding protein F3, and neutrophil cytosolic factor 2 as significantly elevated in rapid amyotrophic lateral sclerosis. Cell type frequency and protein expression, such as T helper 17 cell–interleukin-17A and mature CD8 T cell–killer cell lectin-like receptor D1, were significantly correlated. Conclusions and Relevance: The progression rate was related to the increase of T helper 17 cells versus regulatory T cells and titers of T helper 17 cell- and CD8 T cell-related immunoproteins in patients with amyotrophic lateral sclerosis. These results provide promising biomarkers and targets for amyotrophic lateral sclerosis disease-modifying therapies.
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