ArticleBrain pathology (Zurich, Switzerland)2005
Involvement of clusterin and the aggresome in abnormal protein deposits in myofibrillar myopathies and inclusion body myositis.
Article in Brain pathology (Zurich, Switzerland), 2005. 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, 41 citations in OpenAlex.
- Extracellular chaperone networks and the export of J-domain proteins.The Journal of biological chemistry · 2023Review
- Increased clusterin levels after myocardial infarction is due to a defect in protein degradation systems activity.Cell death & disease · 2019Article
- Development of AD-Like Pathology in Skeletal Muscle.Journal of Parkinson's disease and Alzheimer's disease · 2019Article
- Sisyphus in Neverland.Journal of Alzheimer's disease : JAD · 2018Article
- Clusterin protects neurons against intracellular proteotoxicity.Acta neuropathologica communications · 2017Article
- Intracellular fibril formation, calcification, and enrichment of chaperones, cytoskeletal, and intermediate filament proteins in the adult hippocampus CA1 following neonatal exposure to the nonprotein amino acid BMAA.Archives of toxicology · 2015Article
- Proteasome dysfunction induces muscle growth defects and protein aggregation.Journal of cell science · 2014Article
- Myofibrillar myopathies.Neuromuscular disorders : NMD · 2011Review
- How citation distortions create unfounded authority: analysis of a citation network.BMJ (Clinical research ed.) · 2009Article
- Extralysosomal protein degradation in myofibrillar myopathies.Brain pathology (Zurich, Switzerland) · 2009Review
- Target genes of neuron-restrictive silencer factor are abnormally up-regulated in human myotilinopathy.The American journal of pathology · 2007Article
- Oxidative stress in desminopathies and myotilinopathies: a link between oxidative damage and abnormal protein aggregation.Brain pathology (Zurich, Switzerland) · 2007Article
- Advances in the immunobiology and treatment of inflammatory myopathies.Current rheumatology reports · 2007Review
- Up-regulation of the clusterin gene after proteotoxic stress: implication of HSF1-HSF2 heterocomplexes.The Biochemical journal · 2006Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myofibrillar myopathies (MM) are characterized morphologically by the presence of non-hyaline structures corresponding to foci of dissolution of myofibrils, and hyaline lesions composed of aggregates of compacted and degraded myofibrillar elements. Inclusion body myositis (IBM) is characterized by the presence of rimmed vacuoles, eosinophilic inclusions in the cytoplasm, rare intranuclear inclusions, and by the accumulation of several abnormal proteins. Recent studies have demonstrated impaired proteasomal expression and activity in MM and IBM, thus accounting, in part, for the abnormal protein accumulation in these diseases. The present study examines other factors involved in protein aggregation in MM and IBM. Clusterin is a multiple-function protein which participates in Abeta-amyloid, PrP(res) and a-synuclein aggregation in Alzheimer disease, prionopathies and a-synucleinopathies, respectively. gamma-Tubulin is present in the centrosome and is an intracellular marker of the aggresome. Moderate or strong clusterin immunoreactivity has been found in association with abnormal protein deposits, as revealed by immunohistochemistry, single and double-labeling immunofluorescence and confocal microscopy, in MM and IBM, and in target structures in denervation atrophy. Gamma-Tubulin has also been observed in association with abnormal protein deposits in MM, IBM, and in target fibers in denervation atrophy. These morphological findings are accompanied by increased expression of clusterin and gamma-tubulin in muscle homogenates of MM and IBM cases, as revealed by gel electrophoresis and Western blots. Together, these observations demonstrate involvement of clusterin in protein aggregates, and increased expression of aggresome markers in association with abnormal protein inclusions in MM and IBM and in targets, as crucial events related to the pathogenesis of abnormal protein accumulation and degradation in these muscular diseases.
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