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Analysis of skeletal muscle gene expression upon mouse hindlimb unloading and reloading

ABSTRACT: Analysis of skeletal muscle gene expression upon mouse hindlimb unloading and reloading

PROVIDER: PRJNA993705 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25238416_1.fastq.gz	Fastqsanger.gz
	SRR25238416_2.fastq.gz	Fastqsanger.gz
	SRR25238417_1.fastq.gz	Fastqsanger.gz
	SRR25238417_2.fastq.gz	Fastqsanger.gz
	SRR25238418_1.fastq.gz	Fastqsanger.gz

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Analysis of skeletal muscle gene expression upon mouse hindlimb unloading and reloading

Project description:To investigate the molecular mechanisms governing the transition of skeletal muscle from atrophy to compensatory regeneration and hypertrophy, we employed a mouse model involving hindlimb unloading and subsequent reloading, conducting a comprehensive analysis of global gene expression using RNA-sequencing (RNA-seq). Gastrocnemius muscle samples were obtained from three groups: control mice, mice subjected to 10 days of hindlimb unloading-induced muscle atrophy, and mice reintroduced to normal cage activity for 1 day following the unloading period (reloading).

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Employing Hindlimb Unloading Model for The Identification of Serum Biomarkers Associated with Cardiovascular and Skeletal Muscle Deconditioning.

Project description:Microgravity and prolonged periods of inactivity cause a variety of diseases, including skeletal muscle mass loss and weakening as well as cardiovascular deconditioning. The primary causes of the inadequate preventative measures for these deconditionings are the lack of biomarkers and unknown underlying mechanisms of cardiovascular and skeletal muscle deconditioning in these conditions. Here, we used a hindlimb unloading (HU) mouse model that replicates astronauts in space and bedridden patients to first evaluate cardiovascular and skeletal muscle performance. Serum samples from these mice were used to identify new biomarkers using metabolomic and proteomic approaches. Three weeks of unloading resulted in alterations in cardiovascular system function in C57/Bl6 mice, as measured by changes in mean arterial pressure and heart weight. Unloading for three weeks also altered skeletal muscle function, resulting in a decrease of grip strength in HU mice, as well as skeletal muscle atrophy, as shown by a drop in muscle mass. A two-week recovery time from the unloading condition partially reversed these alterations, stressing the importance of the recovery process.

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Project description:In this work we employed classic skeletal muscle unloading rat model to determine how hindlimb suspension (HS) affects functional activity of skeletal muscle progenitor cells (SMPC). We have purified SMPC from m. soleus from control rats and after 1, 3, 7 and 14 days of exposure (HS1, HS3, HS7, HS14).

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Project description:Examination of effect of mechanical loading induced by hindlimb suspension, and subsequent reloading, in soleus muscle in 14 day old female pathogenâfree Wistar rats. Keywords = skeletal muscle Keywords = atrophy

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Integrated Proteomic and Metabolomic Analysis of Muscle Atrophy Induced by Hindlimb Unloading

Project description:Skeletal muscle atrophy, which is induced by factors such as disuse, spaceflight, certain medications, neurological disorders, and malnutrition, is a global health issue lacking effective treatment. Hindlimb unloading is a commonly used model for muscle atrophy. However, the underlying mechanism of muscle atrophy induced by hindlimb unloading remains unclear, particular from the perspective of myocyte proteome and metabolism. We first used mass spectrometry for proteomic sequencing and untargeted metabolomics to analyze soleus muscle changes in rats with hindlimb unloading. The study found 1052 proteins and 377 metabolites (with MS2 name) differentially expressed between HU group and CON group. Proteins like ACTN3, MYH4, MYBPC2, and MYOZ1, typically found in fast-twitch muscles, were upregulated, along with metabolism-related proteins GLUL, GSTM4, and NDUFS4. Metabolites arachidylcarnitine and 7,8-dihydrobiopterin, and pathways like histidine, taurine, and hypotaurine metabolism were linked to muscle atrophy. Protein and metabolism joint analysis revealed that some pathways such as glutathione metabolism, ferroptosis and lysosome pathways were likely to be involved in soleus atrophy. In this study, we have applied integrated deep proteomic and metabolomic analysis. The upregulation of proteins which are expressed in fast-twitch fibers indicated the conversion of slow-twitch fibers to fast-twitch fibers under HU. Some metabolism-related proteins have been screened out. Besides, some differentially abundant metabolites and pathways revealed the important role of metabolism in the muscle atrophy of soleus. Our study provides insights into the pathogenesis and treatment of muscle atrophy that results from unloading by integrating the proteomics and metabolomics of soleus muscles.

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Project description:Examination of effect of mechanical loading induced by hindlimb suspension, and subsequent reloading, in soleus muscle in 14 day old female pathogen–free Wistar rats. Keywords = skeletal muscle Keywords = atrophy Keywords: other

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