ArticleHistochemistry and cell biology2011
RNA processing is altered in skeletal muscle nuclei of patients affected by myotonic dystrophy.
Article in Histochemistry and cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Cultured myoblasts from patients affected by myotonic dystrophy type 2 exhibit senescence-related features: ultrastructural evidence.European journal of histochemistry : EJH · 2011Trial
- Myotonic dystrophies: an update on clinical features, molecular mechanisms, management, and gene therapy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Myotonic Dystrophies: A Genetic Overview.Genes · 2022Review
- Age-Related Changes in the Matrisome of the Mouse Skeletal Muscle.International journal of molecular sciences · 2021Article
- Review
- Myotonic dystrophy type 2 and modifier genes: an update on clinical and pathomolecular aspects.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Review
- Myotonic Dystrophy Type 2: An Update on Clinical Aspects, Genetic and Pathomolecular Mechanism.Journal of neuromuscular diseases · 2015Article
- Muscle wasting in myotonic dystrophies: a model of premature aging.Frontiers in aging neuroscience · 2015Review
- Premature senescence in primary muscle cultures of myotonic dystrophy type 2 is not associated with p16 induction.European journal of histochemistry : EJH · 2014Article
- RNA Transcription and Maturation in Skeletal Muscle Cells are Similarly Impaired in Myotonic Dystrophy and Sarcopenia: The Ultrastructural Evidence.Frontiers in aging neuroscience · 2014Review
- Histochemistry as an irreplaceable approach for investigating functional cytology and histology.European journal of histochemistry : EJH · 2013Article
- Muscleblind-like1 undergoes ectopic relocation in the nuclei of skeletal muscles in myotonic dystrophy and sarcopenia.European journal of histochemistry : EJH · 2013Article
- Nuclear ribonucleoprotein-containing foci increase in size in non-dividing cells from patients with myotonic dystrophy type 2.Histochemistry and cell biology · 2012Article
- Skeletal muscle features in myotonic dystrophy and sarcopenia: do similar nuclear mechanisms lead to skeletal muscle wasting?European journal of histochemistry : EJH · 2012Review
- Recent progress in histochemistry and cell biology.Histochemistry and cell biology · 2012Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myotonic dystrophies (DMs) are characterised by highly variable clinical manifestations consisting of muscle weakness and atrophy, and a wide spectrum of extramuscular manifestations. In both DM1 and DM2 forms, expanded nucleotide sequences cause the accumulation of mutant transcripts in the nucleus, thus deregulating the function of some RNA-binding proteins and providing a plausible explanation for the multifactorial phenotype of DM patients. However, at the skeletal muscle level, no mechanistic explanation for the muscle wasting has so far been proposed. We therefore performed a study in situ by immunoelectron microscopy on biceps brachii biopsies from DM1, DM2 and healthy subjects, providing the first ultrastructural evidence on the distribution of some nuclear ribonucleoprotein (RNP)-containing structures and molecular factors involved in pre-mRNA transcription and maturation in dystrophic myonuclei. Our results demonstrated an accumulation of splicing and cleavage factors in myonuclei of both DM1 and DM2 patients, suggesting an impairment of post-transcriptional pre-mRNA pathways. The transcription of the expanded sequences in DM myonuclei would therefore hamper functionality of the whole splicing machinery, slowing down the intranuclear molecular trafficking; this would reduce the capability of myonuclei to respond to anabolic stimuli thus contributing to muscle wasting.
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