Establishment of a dexamethasone-induced zebrafish skeletal muscle atrophy model and exploration of its mechanisms
Background: Skeletal muscle atrophy is one of the main side effects of high-dose or continuous use of glucocorticoids (such as dexamethasone). However, there are limited studies on dexamethasone-induced skeletal muscle atrophy in zebrafish and even fewer explorations of the underlying molecular mech...
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Elsevier
2024-12-01
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| Series: | Experimental Gerontology |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0531556524002614 |
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| author | Chen-Chen Sun Ye-Jun Li Dan-Ting Zhu Zhang-Lin Chen Jiang-Ling Xiao Xiang-Tao Chen Lan Zheng Xi-Yang Peng Chang-Fa Tang |
| author_facet | Chen-Chen Sun Ye-Jun Li Dan-Ting Zhu Zhang-Lin Chen Jiang-Ling Xiao Xiang-Tao Chen Lan Zheng Xi-Yang Peng Chang-Fa Tang |
| author_sort | Chen-Chen Sun |
| collection | DOAJ |
| description | Background: Skeletal muscle atrophy is one of the main side effects of high-dose or continuous use of glucocorticoids (such as dexamethasone). However, there are limited studies on dexamethasone-induced skeletal muscle atrophy in zebrafish and even fewer explorations of the underlying molecular mechanisms. This study aimed to construct a model of dexamethasone-induced skeletal muscle atrophy in zebrafish and to investigate the molecular mechanisms. Methods: Zebrafish soaked in 0.01 % dexamethasone solution for 10 days. Loli Track (Denmark) and Loligo Swimming Respirometer were used to observe the effect of dexamethasone on swimming ability. The effects of dexamethasone on zebrafish skeletal muscle were observed by Transmission electron microscopy, H&E, and wheat germ agglutinin techniques. Enriched genes and signaling pathways were analyzed using Transcriptome sequencing. Further, the levels of mitochondrial and endoplasmic reticulum-related proteins were examined to investigate possible mechanisms. Results: 0.01 % dexamethasone reduced zebrafish skeletal muscle mass (p < 0.05), myofibre size and cross-sectional area (p < 0.001), and increased protein degradation (ubiquitination and autophagy) (p < 0.05). In addition, 0.01 % dexamethasone reduced the swimming ability of zebrafish, as evidenced by the reluctance to move, fewer movement trajectories, decreased total distance traveled (p < 0.001), average velocity of movement (p < 0.001), oxygen consumption (p < 0.001), critical swimming speed (p < 0.01) and increased exhaustive swimming time (p < 0.001). Further, 0.01 % dexamethasone-induced mitochondrial dysfunction (decreased mitochondrial biogenesis, disturbs kinetic homeostasis, increased autophagy) and endoplasmic reticulum stress. Conclusions: 0.01 % dexamethasone induces skeletal muscle atrophy and impairs the swimming ability of zebrafish through mitochondrial dysfunction and endoplasmic reticulum stress. |
| format | Article |
| id | doaj-art-10b73c6b7f1a4250bf4b96f5088b945f |
| institution | OA Journals |
| issn | 1873-6815 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Experimental Gerontology |
| spelling | doaj-art-10b73c6b7f1a4250bf4b96f5088b945f2025-08-20T02:10:50ZengElsevierExperimental Gerontology1873-68152024-12-0119811261510.1016/j.exger.2024.112615Establishment of a dexamethasone-induced zebrafish skeletal muscle atrophy model and exploration of its mechanismsChen-Chen Sun0Ye-Jun Li1Dan-Ting Zhu2Zhang-Lin Chen3Jiang-Ling Xiao4Xiang-Tao Chen5Lan Zheng6Xi-Yang Peng7Chang-Fa Tang8Institute of Physical Education, Hunan First Normal University, Changsha, Hunan 410205, China; Key Laboratory of Physical Fitness and Exercise Rehabilitation, State Key Laboratory of Developmental Biology of Freshwater Fish of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha, Hunan 410012, ChinaSchool of Educational Science, Hunan Normal University, Changsha, Hunan 410012, ChinaKey Laboratory of Physical Fitness and Exercise Rehabilitation, State Key Laboratory of Developmental Biology of Freshwater Fish of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha, Hunan 410012, ChinaKey Laboratory of Physical Fitness and Exercise Rehabilitation, State Key Laboratory of Developmental Biology of Freshwater Fish of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha, Hunan 410012, ChinaKey Laboratory of Physical Fitness and Exercise Rehabilitation, State Key Laboratory of Developmental Biology of Freshwater Fish of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha, Hunan 410012, ChinaKey Laboratory of Physical Fitness and Exercise Rehabilitation, State Key Laboratory of Developmental Biology of Freshwater Fish of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha, Hunan 410012, ChinaKey Laboratory of Physical Fitness and Exercise Rehabilitation, State Key Laboratory of Developmental Biology of Freshwater Fish of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha, Hunan 410012, ChinaKey Laboratory of Physical Fitness and Exercise Rehabilitation, State Key Laboratory of Developmental Biology of Freshwater Fish of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha, Hunan 410012, China; Corresponding authors at: Key Laboratory of Physical Fitness and Exercise Rehabilitation of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha, Hunan 410012, China.Key Laboratory of Physical Fitness and Exercise Rehabilitation, State Key Laboratory of Developmental Biology of Freshwater Fish of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha, Hunan 410012, China; Corresponding authors at: Key Laboratory of Physical Fitness and Exercise Rehabilitation of the Hunan Province, College of Physical Education, Hunan Normal University, Changsha, Hunan 410012, China.Background: Skeletal muscle atrophy is one of the main side effects of high-dose or continuous use of glucocorticoids (such as dexamethasone). However, there are limited studies on dexamethasone-induced skeletal muscle atrophy in zebrafish and even fewer explorations of the underlying molecular mechanisms. This study aimed to construct a model of dexamethasone-induced skeletal muscle atrophy in zebrafish and to investigate the molecular mechanisms. Methods: Zebrafish soaked in 0.01 % dexamethasone solution for 10 days. Loli Track (Denmark) and Loligo Swimming Respirometer were used to observe the effect of dexamethasone on swimming ability. The effects of dexamethasone on zebrafish skeletal muscle were observed by Transmission electron microscopy, H&E, and wheat germ agglutinin techniques. Enriched genes and signaling pathways were analyzed using Transcriptome sequencing. Further, the levels of mitochondrial and endoplasmic reticulum-related proteins were examined to investigate possible mechanisms. Results: 0.01 % dexamethasone reduced zebrafish skeletal muscle mass (p < 0.05), myofibre size and cross-sectional area (p < 0.001), and increased protein degradation (ubiquitination and autophagy) (p < 0.05). In addition, 0.01 % dexamethasone reduced the swimming ability of zebrafish, as evidenced by the reluctance to move, fewer movement trajectories, decreased total distance traveled (p < 0.001), average velocity of movement (p < 0.001), oxygen consumption (p < 0.001), critical swimming speed (p < 0.01) and increased exhaustive swimming time (p < 0.001). Further, 0.01 % dexamethasone-induced mitochondrial dysfunction (decreased mitochondrial biogenesis, disturbs kinetic homeostasis, increased autophagy) and endoplasmic reticulum stress. Conclusions: 0.01 % dexamethasone induces skeletal muscle atrophy and impairs the swimming ability of zebrafish through mitochondrial dysfunction and endoplasmic reticulum stress.http://www.sciencedirect.com/science/article/pii/S0531556524002614Skeletal muscle atrophyZebrafishDexamethasoneMitochondrial dysfunctionEndoplasmic reticulum stress |
| spellingShingle | Chen-Chen Sun Ye-Jun Li Dan-Ting Zhu Zhang-Lin Chen Jiang-Ling Xiao Xiang-Tao Chen Lan Zheng Xi-Yang Peng Chang-Fa Tang Establishment of a dexamethasone-induced zebrafish skeletal muscle atrophy model and exploration of its mechanisms Experimental Gerontology Skeletal muscle atrophy Zebrafish Dexamethasone Mitochondrial dysfunction Endoplasmic reticulum stress |
| title | Establishment of a dexamethasone-induced zebrafish skeletal muscle atrophy model and exploration of its mechanisms |
| title_full | Establishment of a dexamethasone-induced zebrafish skeletal muscle atrophy model and exploration of its mechanisms |
| title_fullStr | Establishment of a dexamethasone-induced zebrafish skeletal muscle atrophy model and exploration of its mechanisms |
| title_full_unstemmed | Establishment of a dexamethasone-induced zebrafish skeletal muscle atrophy model and exploration of its mechanisms |
| title_short | Establishment of a dexamethasone-induced zebrafish skeletal muscle atrophy model and exploration of its mechanisms |
| title_sort | establishment of a dexamethasone induced zebrafish skeletal muscle atrophy model and exploration of its mechanisms |
| topic | Skeletal muscle atrophy Zebrafish Dexamethasone Mitochondrial dysfunction Endoplasmic reticulum stress |
| url | http://www.sciencedirect.com/science/article/pii/S0531556524002614 |
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