ArticlePloS one2012
Analysis of the fibroblast growth factor system reveals alterations in a mouse model of spinal muscular atrophy.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- MyomiR Networks in Spinal Muscular Atrophy: Associations With Clinical Severity and Treatment Response.Molecular neurobiology · 2026Article
- bootGSEA: a bootstrap and rank aggregation pipeline for multi-study and multi-omics enrichment analyses.Frontiers in bioinformatics · 2024Article
- Spinal astrocyte dysfunction drives motor neuron loss in late-onset spinal muscular atrophy.Acta neuropathologica · 2023Article
- Culture Conditions for Human Induced Pluripotent Stem Cell-Derived Schwann Cells: A Two-Centre Study.International journal of molecular sciences · 2023Article
- Drug Discovery of Spinal Muscular Atrophy (SMA) from the Computational Perspective: A Comprehensive Review.International journal of molecular sciences · 2021Review
- Modified Hyaluronic Acid-Laminin-Hydrogel as Luminal Filler for Clinically Approved Hollow Nerve Guides in a Rat Critical Defect Size Model.International journal of molecular sciences · 2021Article
- Impairment of the neurotrophic signaling hub B-Raf contributes to motoneuron degeneration in spinal muscular atrophy.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- What Can We Learn from FGF-2 Isoform-Specific Mouse Mutants? Differential Insights into FGF-2 Physiology In Vivo.International journal of molecular sciences · 2020Review
- A Single Amino Acid Residue Regulates PTEN-Binding and Stability of the Spinal Muscular Atrophy Protein SMN.Cells · 2020Article
- The Need for SMN-Independent Treatments of Spinal Muscular Atrophy (SMA) to Complement SMN-Enhancing Drugs.Frontiers in neurology · 2020Review
- Intact interleukin-10 receptor signaling protects from hippocampal damage elicited by experimental neurotropic virus infection of SJL mice.Scientific reports · 2018Article
- Calsenilin, a Presenilin Interactor, Regulates RhoA Signaling and Neurite Outgrowth.International journal of molecular sciences · 2018Article
- Oligodendroglial fibroblast growth factor receptor 1 gene targeting protects mice from experimental autoimmune encephalomyelitis through ERK/AKT phosphorylation.Brain pathology (Zurich, Switzerland) · 2018Article
- Lack of Fgf18 causes abnormal clustering of motor nerve terminals at the neuromuscular junction with reduced acetylcholine receptor clusters.Scientific reports · 2018Article
- Regulation of RhoA activity by the cellular prion protein.Cell death & disease · 2017Article
- Molecular Mechanisms of Neurodegeneration in Spinal Muscular Atrophy.Journal of experimental neuroscience · 2016Review
- A nuclear odyssey: fibroblast growth factor-2 (FGF-2) as a regulator of nuclear homeostasis in the nervous system.Cellular and molecular life sciences : CMLS · 2015Review
- Chatting with the neighbors: crosstalk between Rho-kinase (ROCK) and other signaling pathways for treatment of neurological disorders.Frontiers in neuroscience · 2015Review
- Shared mechanisms between Drosophila peripheral nervous system development and human neurodegenerative diseases.Current opinion in neurobiology · 2014Review
- Genetic circuitry of Survival motor neuron, the gene underlying spinal muscular atrophy.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The monogenetic disease Spinal Muscular Atrophy (SMA) is characterized by a progressive loss of motoneurons leading to muscle weakness and atrophy due to severe reduction of the Survival of Motoneuron (SMN) protein. Several models of SMA show deficits in neurite outgrowth and maintenance of neuromuscular junction (NMJ) structure. Survival of motoneurons, axonal outgrowth and formation of NMJ is controlled by neurotrophic factors such as the Fibroblast Growth Factor (FGF) system. Besides their classical role as extracellular ligands, some FGFs exert also intracellular functions controlling neuronal differentiation. We have previously shown that intracellular FGF-2 binds to SMN and regulates the number of a subtype of nuclear bodies which are reduced in SMA patients. In the light of these findings, we systematically analyzed the FGF-system comprising five canonical receptors and 22 ligands in a severe mouse model of SMA. In this study, we demonstrate widespread alterations of the FGF-system in both muscle and spinal cord. Importantly, FGF-receptor 1 is upregulated in spinal cord at a pre-symptomatic stage as well as in a mouse motoneuron-like cell-line NSC34 based model of SMA. Consistent with that, phosphorylations of FGFR-downstream targets Akt and ERK are increased. Moreover, ERK hyper-phosphorylation is functionally linked to FGFR-1 as revealed by receptor inhibition experiments. Our study shows that the FGF system is dysregulated at an early stage in SMA and may contribute to the SMA pathogenesis.
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