ArticleThe Kaohsiung journal of medical sciences2014
Survival of motor neuron protein downregulates miR-9 expression in patients with spinal muscular atrophy.
Article in The Kaohsiung journal of medical sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- SMN promotes mitochondrial metabolic maturation during myogenesis by regulating the MYOD-miRNA axis.Life science alliance · 2023Article
- The SMN Complex at the Crossroad between RNA Metabolism and Neurodegeneration.International journal of molecular sciences · 2023Review
- Role of circulating biomarkers in spinal muscular atrophy: insights from a new treatment era.Frontiers in neurology · 2023Review
- RNA in spinal muscular atrophy: therapeutic implications of targeting.Expert opinion on therapeutic targets · 2020Review
- miR-206 Reduces the Severity of Motor Neuron Degeneration in the Facial Nuclei of the Brainstem in a Mouse Model of SMA.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Circulating microRNAs as potential biomarkers and therapeutic targets in spinal muscular atrophy.Therapeutic advances in neurological disorders · 2020Review
- AAV9-mediated delivery of miR-23a reduces disease severity in Smn2B/-SMA model mice.Human molecular genetics · 2019Article
- Dysregulation of microRNA metabolism in motor neuron diseases: Novel biomarkers and potential therapeutics.Non-coding RNA research · 2019Review
- miRNA in spinal muscular atrophy pathogenesis and therapy.Journal of cellular and molecular medicine · 2018Review
- Article
- Diverse role of survival motor neuron protein.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017Review
- MotomiRs: miRNAs in Motor Neuron Function and Disease.Frontiers in molecular neuroscience · 2017Review
- Altered Levels of MicroRNA-9, -206, and -132 in Spinal Muscular Atrophy and Their Response to Antisense Oligonucleotide Therapy.Molecular therapy. Nucleic acids · 2016Article
- Neuromuscular Junctions as Key Contributors and Therapeutic Targets in Spinal Muscular Atrophy.Frontiers in neuroanatomy · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal muscular atrophy (SMA) is a lethal hereditary disease caused by homozygous absence of the survival of the motor neuron (SMN) 1 gene (SMN1), and it is the leading genetic cause of infant mortality. The severity of SMA is directly correlated with SMN protein levels in affected patients; however, the cellular regulatory mechanisms for SMN protein expression are not completely understood. In this study, we investigated the regulatory effects between SMN expression and miR-9a, a downstream noncoding small RNA. Using an inducible SMN short hairpin RNA interference (shRNAi) system in NSC 34 and human skin fibroblast cells, cellular miR-9 levels and SMN protein repression were time-dependently upregulated. Conversely, cellular miR-9 levels decreased when HeLa cells were transfected with SMN protein fused with green fluorescent protein. In SMA-like mice spinal cords and human primary skin fibroblasts isolated from patients with different degrees of SMA, human SMN exhibited a disease severity-dependent decrease, whereas cellular miR-9 levels increased. These results clearly suggested that cellular SMN proteins regulated miR-9 expression and that miR-9 expression was related to SMA severity. Thus, miR-9 may be a marker for SMA prognosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.