Hypoxia treatment and resistance training alters microRNA profiling in rats skeletal muscle
Abstract MicroRNAs (miRNAs) may play a crucial regulatory role in the process of muscle atrophy induced by high-altitude hypoxia and its amelioration through resistance training. However, research in this aspect is still lacking. Therefore, this study aimed to employ miRNA microarray analysis to inv...
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2024-04-01
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| Series: | Scientific Reports |
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| Online Access: | https://doi.org/10.1038/s41598-024-58996-7 |
| _version_ | 1797209384578711552 |
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| author | Tao Mei Yang Hu Ying Zhang Yanchun Li |
| author_facet | Tao Mei Yang Hu Ying Zhang Yanchun Li |
| author_sort | Tao Mei |
| collection | DOAJ |
| description | Abstract MicroRNAs (miRNAs) may play a crucial regulatory role in the process of muscle atrophy induced by high-altitude hypoxia and its amelioration through resistance training. However, research in this aspect is still lacking. Therefore, this study aimed to employ miRNA microarray analysis to investigate the expression profile of miRNAs in skeletal muscle from an animal model of hypoxia-induced muscle atrophy and resistance training aimed at mitigating muscle atrophy. The study utilized a simulated hypoxic environment (oxygen concentration at 11.2%) to induce muscle atrophy and established a rat model of resistance training using ladder climbing, with a total intervention period of 4 weeks. The miRNA expression profile revealed 9 differentially expressed miRNAs influenced by hypoxia (e.g., miR-341, miR-32-5p, miR-465-5p) and 14 differentially expressed miRNAs influenced by resistance training under hypoxic conditions (e.g., miR-338-5p, miR-203a-3p, miR-92b-3p) (∣log2(FC)∣ ≥ 1.5, p < 0.05). The differentially expressed miRNAs were found to target genes involved in muscle protein synthesis and degradation (such as Utrn, mdm2, eIF4E), biological processes (such as negative regulation of transcription from RNA polymerase II promoter, regulation of transcription, DNA-dependent), and signaling pathways (such as Wnt signaling pathway, MAPK signaling pathway, ubiquitin-mediated proteolysis, mTOR signaling pathway). This study provides a foundation for understanding and further exploring the molecular mechanisms underlying hypoxia-induced rats muscle atrophy and the mitigation of atrophy through resistance training. |
| first_indexed | 2024-04-24T09:53:51Z |
| format | Article |
| id | doaj.art-fd6e182a827847c78a4a0422c9f53093 |
| institution | Directory Open Access Journal |
| issn | 2045-2322 |
| language | English |
| last_indexed | 2024-04-24T09:53:51Z |
| publishDate | 2024-04-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Reports |
| spelling | doaj.art-fd6e182a827847c78a4a0422c9f530932024-04-14T11:16:33ZengNature PortfolioScientific Reports2045-23222024-04-0114111310.1038/s41598-024-58996-7Hypoxia treatment and resistance training alters microRNA profiling in rats skeletal muscleTao Mei0Yang Hu1Ying Zhang2Yanchun Li3China Institute of Sport and Health Science, Beijing Sport UniversityChina Institute of Sport and Health Science, Beijing Sport UniversityChina Institute of Sport and Health Science, Beijing Sport UniversityChina Institute of Sport and Health Science, Beijing Sport UniversityAbstract MicroRNAs (miRNAs) may play a crucial regulatory role in the process of muscle atrophy induced by high-altitude hypoxia and its amelioration through resistance training. However, research in this aspect is still lacking. Therefore, this study aimed to employ miRNA microarray analysis to investigate the expression profile of miRNAs in skeletal muscle from an animal model of hypoxia-induced muscle atrophy and resistance training aimed at mitigating muscle atrophy. The study utilized a simulated hypoxic environment (oxygen concentration at 11.2%) to induce muscle atrophy and established a rat model of resistance training using ladder climbing, with a total intervention period of 4 weeks. The miRNA expression profile revealed 9 differentially expressed miRNAs influenced by hypoxia (e.g., miR-341, miR-32-5p, miR-465-5p) and 14 differentially expressed miRNAs influenced by resistance training under hypoxic conditions (e.g., miR-338-5p, miR-203a-3p, miR-92b-3p) (∣log2(FC)∣ ≥ 1.5, p < 0.05). The differentially expressed miRNAs were found to target genes involved in muscle protein synthesis and degradation (such as Utrn, mdm2, eIF4E), biological processes (such as negative regulation of transcription from RNA polymerase II promoter, regulation of transcription, DNA-dependent), and signaling pathways (such as Wnt signaling pathway, MAPK signaling pathway, ubiquitin-mediated proteolysis, mTOR signaling pathway). This study provides a foundation for understanding and further exploring the molecular mechanisms underlying hypoxia-induced rats muscle atrophy and the mitigation of atrophy through resistance training.https://doi.org/10.1038/s41598-024-58996-7HypoxiaResistance trainingSkeletal muscle atrophyMiRNA expression profileBioinformatics analysis |
| spellingShingle | Tao Mei Yang Hu Ying Zhang Yanchun Li Hypoxia treatment and resistance training alters microRNA profiling in rats skeletal muscle Scientific Reports Hypoxia Resistance training Skeletal muscle atrophy MiRNA expression profile Bioinformatics analysis |
| title | Hypoxia treatment and resistance training alters microRNA profiling in rats skeletal muscle |
| title_full | Hypoxia treatment and resistance training alters microRNA profiling in rats skeletal muscle |
| title_fullStr | Hypoxia treatment and resistance training alters microRNA profiling in rats skeletal muscle |
| title_full_unstemmed | Hypoxia treatment and resistance training alters microRNA profiling in rats skeletal muscle |
| title_short | Hypoxia treatment and resistance training alters microRNA profiling in rats skeletal muscle |
| title_sort | hypoxia treatment and resistance training alters microrna profiling in rats skeletal muscle |
| topic | Hypoxia Resistance training Skeletal muscle atrophy MiRNA expression profile Bioinformatics analysis |
| url | https://doi.org/10.1038/s41598-024-58996-7 |
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