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Our study is the first to demonstrate the ability to generate iPS cells from a mouse model of Pompe disease. Initially, mouse tail tip fibroblasts were harvested from male, 8-week-old (GAA) knockout mice, and three reprogramming factors (Oct3/4, Sox2 and Klf4) were transfected into the isolated donor cells using a retroviral vector. These iPS cells also showed decreased levels of GAA enzymatic activity and strong positive staining with periodic acid-Schiff (indicating the accumulation of glycogen) and acid phosphatase (lysosomal activation marker). Pompe-iPS cells were differentiated into skeletal muscle cells in Matrigel®-coated plates. Spindle-shaped skeletal muscle cells were successfully generated from Pompe-iPS cells and showed spontaneous contraction and positive staining with the myosin heavy chain antibody. Electron microscopic analysis of the skeletal muscle cells showed typical morphological features, including Z-bands, I-bands, A-bands and H-bands, which were visible in wild-type and Pompe cells. Furthermore, Pompe skeletal muscle cells accumulated massive glycogen in lysosomes. This study indicates that the iPS and skeletal muscle cells generated in this study could also be a useful disease model for studies investigating the pathogenesis and treatment of skeletal muscle in Pompe disease.
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http://dx.doi.org/10.1016/j.ymgme.2011.05.020 | DOI Listing |
Am J Forensic Med Pathol
September 2025
Department of Pathology, St Louis University School of Medicine, Office of the Medical Examiner - City of St. Louis, St. Louis, MO.
Myotonic dystrophy type 1, or dystrophia myotonica type 1 (DM1), is a multisystem disorder inherited in an autosomal dominant manner. It is caused by a CTG tri-nucleotide expansion in the 3'-untranslated region (3'-UTR) of the dystrophia myotonia protein kinase (DMPK) gene. Core clinical features include progressive skeletal muscle weakness, myotonia, and systemic complications, with premature mortality most often due to respiratory or cardiac dysfunction.
View Article and Find Full Text PDFNeuropathol Appl Neurobiol
October 2025
Division of Rheumatology and Systemic Inflammatory Diseases, III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Aims: Sarcoid myopathy (SaM) is characterised by granulomatous myositis (GM) and can overlap with inclusion body myositis (IBM), a late-onset chronic idiopathic inflammatory myopathy with a still enigmatic pathogenesis. As GM can occur in different clinical contexts, we aimed to examine the histomorphologic features and gene expression profiles in cases of definite SaM that may inform diagnostic and therapeutic considerations.
Methods: We performed a multidimensional characterisation of muscle biopsy specimens from patients with 'pure SaM' (n=17), SaM with concomitant IBM (SaM-IBM) (n=2), including histopathologic and ultrastructural analysis in addition to quantitative real-time polymerase chain reaction.
J Cachexia Sarcopenia Muscle
October 2025
Department of Sports Science, College of Natural Science, Jeonbuk National University, Jeonju, Republic of Korea.
Background: Fine particulate matter has developmental toxicity, and midgestation is an important period for the development of foetal skeletal muscle. The ability of exercise to modulate skeletal muscle damage in mice exposed to PM during gestation remains unclear.
Methods: Pregnant C57BL/6 mice were exposed to 50 μg/m PM for 2 h on five consecutive days starting at embryonic day 12.
J Endocrinol
September 2025
University of Missouri, Columbia, MO.
Purpose: CL316,243 (CL), a beta 3 adrenergic receptor (B3-AR) agonist has 'exercise mimetic' effects in adipose tissue (AT). CL may also positively affect skeletal muscle (SM), yet the role of estrogen receptor beta (ERβ) in mediating SM-specific effects of CL is not known. We investigated the effects of CL on SM metabolism, as well as the role played by ERβ.
View Article and Find Full Text PDFMol Ther Methods Clin Dev
June 2025
Université Paris-Saclay, University Evry, Inserm, Genethon, Integrare Research Unit UMR_S951, 91000 Evry, France.
Pompe disease is a glycogen storage disorder caused by mutations in the acid α-glucosidase (GAA) gene, leading to reduced GAA activity and glycogen accumulation in heart and skeletal muscles. Enzyme replacement therapy with recombinant GAA, the standard of care for Pompe disease, is limited by poor skeletal muscle distribution and immune responses after repeated administrations. The expression of GAA in muscle with adeno-associated virus (AAV) vectors has shown limitations, mainly the low targeting efficiency and immune responses to the transgene.
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