ArticleCellular and molecular neurobiology2014
Early gene expression changes in skeletal muscle from SOD1(G93A) amyotrophic lateral sclerosis animal model.
Article in Cellular and molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Bibliometric analysis and core target identification of network pharmacology on neuroinflammation in central nervous system disorders: Trends, collaborations, and future directions.Neuroprotection (Chichester, England) · 2025Review
- New perspectives of the role of skeletal muscle derived extracellular vesicles in the pathogenesis of amyotrophic lateral sclerosis: the 'dying back' hypothesis.Journal of extracellular biology · 2024Review
- Lysyl oxidase-like 2 inhibitor rescues D-galactose-induced skeletal muscle fibrosis.Aging cell · 2022Article
- Inhibition of myostatin and related signaling pathways for the treatment of muscle atrophy in motor neuron diseases.Cellular and molecular life sciences : CMLS · 2022Review
- Review
- Downregulation of RIPK4 Expression Inhibits Epithelial-Mesenchymal Transition in Ovarian Cancer through IL-6.Journal of immunology research · 2021Article
- Neuromuscular Development and Disease: Learning FromFrontiers in cell and developmental biology · 2021Review
- Transcriptomics and Metabolomics in Amyotrophic Lateral Sclerosis.Advances in experimental medicine and biology · 2020Review
- Wnt Signaling Alterations in the Human Spinal Cord of Amyotrophic Lateral Sclerosis Cases: Spotlight on Fz2 and Wnt5a.Molecular neurobiology · 2019Article
- Inhibition of p70 S6 kinase activity by A77 1726 induces autophagy and enhances the degradation of superoxide dismutase 1 (SOD1) protein aggregates.Cell death & disease · 2018Article
- Inhibition of Drp1/Fis1 interaction slows progression of amyotrophic lateral sclerosis.EMBO molecular medicine · 2018Article
- ALS-Associated Endoplasmic Reticulum Proteins in Denervated Skeletal Muscle: Implications for Motor Neuron Disease Pathology.Brain pathology (Zurich, Switzerland) · 2017Article
- The Role of Skeletal Muscle in Amyotrophic Lateral Sclerosis.Brain pathology (Zurich, Switzerland) · 2016Review
- Dysregulated expression of death, stress and mitochondrion related genes in the sciatic nerve of presymptomatic SOD1(G93A) mouse model of Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2015Article
- Gene expression profiling for human iPS-derived motor neurons from sporadic ALS patients reveals a strong association between mitochondrial functions and neurodegeneration.Frontiers in cellular neuroscience · 2015Article
- Intricate effects of primary motor neuronopathy on contractile proteins and metabolic muscle enzymes as revealed by label-free mass spectrometry.Bioscience reports · 2014Article
- Deregulated expression of cytoskeleton related genes in the spinal cord and sciatic nerve of presymptomatic SOD1(G93A) Amyotrophic Lateral Sclerosis mouse model.Frontiers in cellular neuroscience · 2014Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by loss of motor neurons. Familial ALS is strongly associated to dominant mutations in the gene for Cu/Zn superoxide dismutase (SOD1). Recent evidences point to skeletal muscle as a primary target in the ALS mouse model. Wnt/PI3 K signaling pathways and epithelial-mesenchymal transition (EMT) have important roles in maintenance and repair of skeletal muscle. Wnt/PI3 K pathways and EMT gene expression profile were investigated in gastrocnemius muscle from SOD1(G93A) mouse model and age-paired wild-type control in the presymptomatic ages of 40 and 80 days aiming the early neuromuscular abnormalities that precede motor neuron death in ALS. A customized cDNA microarray platform containing 326 genes of Wnt/PI3 K and EMT was used and results revealed eight up-regulated (Loxl2, Pik4ca, Fzd9, Cul1, Ctnnd1, Snf1lk, Prkx, Dner) and nine down-regulated (Pik3c2a, Ripk4, Id2, C1qdc1, Eif2ak2, Rac3, Cds1, Inppl1, Tbl1x) genes at 40 days, and also one up-regulated (Pik3ca) and five down-regulated (Cd44, Eef2 k, Fzd2, Crebbp, Piki3r1) genes at 80 days. Also, protein-protein interaction networks grown from the differentially expressed genes of 40 and 80 days old mice have identified Grb2 and Src genes in both presymptomatic ages, thus playing a potential central role in the disease mechanisms. mRNA and protein levels for Grb2 and Src were found to be increased in 80 days old ALS mice. Gene expression changes in the skeletal muscle of transgenic ALS mice at presymptomatic periods of disease gave further evidence of early neuromuscular abnormalities that precede motor neuron death. The results were discussed in terms of initial triggering for neuronal degeneration and muscle adaptation to keep function before the onset of symptoms.
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