دورية أكاديمية
Cathelicidin‐related antimicrobial peptide mediates skeletal muscle degeneration caused by injury and Duchenne muscular dystrophy in mice
| العنوان: | Cathelicidin‐related antimicrobial peptide mediates skeletal muscle degeneration caused by injury and Duchenne muscular dystrophy in mice |
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| المؤلفون: | Moon‐Chang Choi, Jiwon Jo, Myeongjin Lee, Jonggwan Park, Tso‐Pang Yao, Yoonkyung Park |
| المصدر: | Journal of Cachexia, Sarcopenia and Muscle, Vol 13, Iss 6, Pp 3091-3105 (2022) |
| بيانات النشر: | Wiley, 2022. |
| سنة النشر: | 2022 |
| المجموعة: | LCC:Diseases of the musculoskeletal system LCC:Human anatomy |
| مصطلحات موضوعية: | Cathelicidin, Cramp, Duchenne muscular dystrophy, Muscle degeneration, Serca1, Diseases of the musculoskeletal system, RC925-935, Human anatomy, QM1-695 |
| الوصف: | Abstract Background Cathelicidin, an antimicrobial peptide, plays a key role in regulating bacterial killing and innate immunity; however, its role in skeletal muscle function is unknown. We investigated the potential role of cathelicidin in skeletal muscle pathology resulting from acute injury and Duchenne muscular dystrophy (DMD) in mice. Methods Expression changes and muscular localization of mouse cathelicidin‐related antimicrobial peptide (Cramp) were examined in the skeletal muscle of normal mice treated with chemicals (cardiotoxin and BaCl2) or in dystrophic muscle of DMD mouse models (mdx, mdx/Utrn+/− and mdx/Utrn−/−). Cramp penetration into myofibres and effects on muscle damage were studied by treating synthetic peptides to mouse skeletal muscles or C2C12 myotubes. Cramp knockout (KO) mice and mdx/Utrn/Cramp KO lines were used to determine whether Cramp mediates muscle degeneration. Muscle pathophysiology was assessed by histological methods, serum analysis, grip strength and lifespan. Molecular factors targeted by Cramp were identified by the pull‐down assay and proteomic analysis. Results In response to acute muscle injury, Cramp was activated in muscle‐infiltrating neutrophils and internalized into myofibres. Cramp treatments of mouse skeletal muscles or C2C12 myotubes resulted in muscle degeneration and myotube damage, respectively. Genetic ablation of Cramp reduced neutrophil infiltration and ameliorated muscle pathology, such as fibre size (P |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 2190-6009 2190-5991 |
| Relation: | https://doaj.org/toc/2190-5991; https://doaj.org/toc/2190-6009 |
| DOI: | 10.1002/jcsm.13065 |
| URL الوصول: | https://doaj.org/article/6e51a23d7f724fb49082d5cc354c302a |
| رقم الأكسشن: | edsdoj.6e51a23d7f724fb49082d5cc354c302a |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 21906009 21905991 |
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| DOI: | 10.1002/jcsm.13065 |