ArticleInternational journal of molecular sciences2013
Notch signaling pathway is activated in motoneurons of spinal muscular atrophy.
Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Neuroanatomical and neurochemical atlas of the spiny mouse (Acomys cahirinus) spinal cord.Brain structure & function · 2025Article
- Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications.Neurology international · 2025Review
- Genetic Variability in Oxidative Stress, Inflammatory, and Neurodevelopmental Pathways: Impact on the Susceptibility and Course of Spinal Muscular Atrophy.Cellular and molecular neurobiology · 2024Article
- Protein expression reveals a molecular sexual identity of avian primordial germ cells at pre-gonadal stages.Scientific reports · 2021Article
- Adipose mesenchymal stem cell transplantation alleviates spinal cord injury-induced neuroinflammation partly by suppressing the Jagged1/Notch pathway.Stem cell research & therapy · 2020Article
- Dominant mutations of the Notch ligand Jagged1 cause peripheral neuropathy.The Journal of clinical investigation · 2020Article
- Notch Signaling Mediates Astrocyte Abnormality in Spinal Muscular Atrophy Model Systems.Scientific reports · 2019Article
- Transcriptome profiling of spinal muscular atrophy motor neurons derived from mouse embryonic stem cells.PloS one · 2014Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal muscular atrophy (SMA) is a neurodegenerative disease produced by low levels of Survival Motor Neuron (SMN) protein that affects alpha motoneurons in the spinal cord. Notch signaling is a cell-cell communication system well known as a master regulator of neural development, but also with important roles in the adult central nervous system. Aberrant Notch function is associated with several developmental neurological disorders; however, the potential implication of the Notch pathway in SMA pathogenesis has not been studied yet. We report here that SMN deficiency, induced in the astroglioma cell line U87MG after lentiviral transduction with a shSMN construct, was associated with an increase in the expression of the main components of Notch signaling pathway, namely its ligands, Jagged1 and Delta1, the Notch receptor and its active intracellular form (NICD). In the SMNΔ7 mouse model of SMA we also found increased astrocyte processes positive for Jagged1 and Delta1 in intimate contact with lumbar spinal cord motoneurons. In these motoneurons an increased Notch signaling was found, as denoted by increased NICD levels and reduced expression of the proneural gene neurogenin 3, whose transcription is negatively regulated by Notch. Together, these findings may be relevant to understand some pathologic attributes of SMA motoneurons.
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