scholarly journals Muscle Satellite Cells and Duchenne Muscular Dystrophy

10.5772/30769 ◽  
2012 ◽  
Author(s):  
Yuko Miyagoe-Suzuki ◽  
So-ichiro Fukada ◽  
Shinichi Take
Keyword(s):  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Satellite Cells ◽  
Muscle Satellite Cells

scholarly journals Satellite Cells: Regenerative Mechanisms and Applicability in Muscular Dystrophy

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Gustavo Torres de Souza ◽  
Rafaella de Souza Salomão Zanette ◽  
Danielle Luciana Aurora Soares do Amaral ◽  
Francisco Carlos da Guia ◽  
Claudinéia Pereira Maranduba ◽  
...  
Keyword(s):  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Cell Population ◽  
Satellite Cells ◽  
Specific Pattern ◽  
Cell Populations ◽  
Heterogeneous Cell Population ◽  
Factor Expression ◽  
Transcription Factor Expression ◽  
Severe Tissue

The satellite cells are long regarded as heterogeneous cell population, which is intimately linked to the processes of muscular recovery. The heterogeneous cell population may be classified by specific markers. In spite of the significant amount of variation amongst the satellite cell populations, it seems that their activity is tightly bound to the paired box 7 transcription factor expression, which is, therefore, used as a canonical marker for these cells. Muscular dystrophic diseases, such as Duchenne muscular dystrophy, elicit severe tissue injuries leading those patients to display a very specific pattern of muscular recovery abnormalities. There have been works on the application of precursors cells as a therapeutic alternative for Duchenne muscular dystrophy and initial attempts have proven the cells inefficient; however later endeavours have proposed solutions for the experiments improving significantly the results. The presence of a range of satellite cells populations indicates the existence of specific cells with enhanced capability of muscular recovery in afflicted muscles.

Heme Oxygenase-1 Influences Satellite Cells and Progression of Duchenne Muscular Dystrophy in Mice

2018 ◽  
Vol 29 (2) ◽  
pp. 128-148 ◽  
Author(s):  
Katarzyna Pietraszek-Gremplewicz ◽  
Magdalena Kozakowska ◽  
Iwona Bronisz-Budzynska ◽  
Maciej Ciesla ◽  
Olga Mucha ◽  
...  
Keyword(s):  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Heme Oxygenase ◽  
Satellite Cells ◽  
Heme Oxygenase 1

scholarly journals Cellular senescence-mediated exacerbation of Duchenne muscular dystrophy

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Hidetoshi Sugihara ◽  
Naomi Teramoto ◽  
Katsuyuki Nakamura ◽  
Takanori Shiga ◽  
Taku Shirakawa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Muscle Strength ◽  
Progenitor Cells ◽  
Satellite Cells ◽  
Muscle Regeneration ◽  
Mesenchymal Progenitor Cells

Abstract Duchenne muscular dystrophy (DMD) is a progressive disease characterised by chronic muscle degeneration and inflammation. Our previously established DMD model rats (DMD rats) have a more severe disease phenotype than the broadly used mouse model. We aimed to investigate the role of senescence in DMD using DMD rats and patients. Senescence was induced in satellite cells and mesenchymal progenitor cells, owing to the increased expression of CDKN2A, p16- and p19-encoding gene. Genetic ablation of p16 in DMD rats dramatically restored body weight and muscle strength. Histological analysis showed a reduction of fibrotic and adipose tissues invading skeletal muscle, with increased muscle regeneration. Senolytic drug ABT263 prevented loss of body weight and muscle strength, and increased muscle regeneration in rats even at 8 months—the late stage of DMD. Moreover, senescence markers were highly expressed in the skeletal muscle of DMD patients. In situ hybridization of CDKN2A confirmed the expression of it in satellite cells and mesenchymal progenitor cells in patients with DMD. Collectively, these data provide new insights into the integral role of senescence in DMD progression.

scholarly journals Epigenetic modifications in muscle regeneration and progression of Duchenne muscular dystrophy

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Anna Rugowska ◽  
Alicja Starosta ◽  
Patryk Konieczny
Keyword(s):  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Satellite Cells ◽  
Muscle Regeneration ◽  
Mutation Site ◽  
Muscle Stem Cell ◽  
Regulatory Processes ◽  
Dystrophin Expression ◽  
Oxide Synthase ◽  
Stem Cell Pool

AbstractDuchenne muscular dystrophy (DMD) is a multisystemic disorder that affects 1:5000 boys. The severity of the phenotype varies dependent on the mutation site in the DMD gene and the resultant dystrophin expression profile. In skeletal muscle, dystrophin loss is associated with the disintegration of myofibers and their ineffective regeneration due to defective expansion and differentiation of the muscle stem cell pool. Some of these phenotypic alterations stem from the dystrophin absence-mediated serine–threonine protein kinase 2 (MARK2) misplacement/downregulation in activated muscle stem (satellite) cells and neuronal nitric oxide synthase loss in cells committed to myogenesis. Here, we trace changes in DNA methylation, histone modifications, and expression of regulatory noncoding RNAs during muscle regeneration, from the stage of satellite cells to myofibers. Furthermore, we describe the abrogation of these epigenetic regulatory processes due to changes in signal transduction in DMD and point to therapeutic treatments increasing the regenerative potential of diseased muscles based on this acquired knowledge.

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