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Gene expression of soleus response to simulated microgravity

ABSTRACT: Identification of gravisensitive gene expression in rat soleus muscle exposed to 7 and 14 days of Hindlimb suspension (HS) simulated microgravity. Microgravity causes muscle atrophy possibly due to muscle wasting overtake regeneration. Results provide insight into the molecular mechanisms regulating muscle atrophy. The expression of 787 (373 upregulated and 414 downregulated) and 923 (491 upregulated and 432 downregulated) genes out of 28000 was altered respectively at least 2-fold of 7 and 14 days TS, which represented 397 (233 upregulated and 164 downregulated) genes of common alteration. By using real-time PCR assays, we verified the microarray data using some of the expected genes.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE52056 | GEO | 2013/11/05

SECONDARY ACCESSION(S): PRJNA226596

REPOSITORIES: GEO

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Gene expression of soleus response to simulated microgravity

Project description:Identification of gravisensitive gene expression in rat soleus muscle exposed to 7 and 14 days of Hindlimb suspension (HS) simulated microgravity. Microgravity causes muscle atrophy possibly due to muscle wasting overtake regeneration. Results provide insight into the molecular mechanisms regulating muscle atrophy. The expression of 787 (373 upregulated and 414 downregulated) and 923 (491 upregulated and 432 downregulated) genes out of 28000 was altered respectively at least 2-fold of 7 and 14 days TS, which represented 397 (233 upregulated and 164 downregulated) genes of common alteration. By using real-time PCR assays, we verified the microarray data using some of the expected genes. The tissue was collected from Sprague-Dawley rats (8 weeks of age) subjected to 7, 14days of TS. mRNA expression profile was determined in three groups: control (CN), TS for 7 days (TS-7), and TS for 14 days (TS-14).Three mRNA microarray chips were analyzed for mixture of four samples of each of the three groups.

2013-11-05 | E-GEOD-52056 | biostudies-arrayexpress

miRNAs expression of soleus response to simulated microgravity

2013-11-05 | GSE52055 | GEO

Expression profiling of soleus muscle under the effect of simulated spaceflight

Project description:Spaceflight imposes the risk of skeletal muscle atrophy for astronauts. The understanding of muscle atrophy because of spaceflight is limited, but continued efforts are essential for developing countermeasures of this effect. A distinct difference between spaceflight-induced muscle atrophy and other forms of atrophy is the additional effect of cosmic rays in outer space. To study spaceflight-induced muscle atrophy, we performed two ground-based models of microgravity in a low dose radiation environment and studied transcriptional changes in rat soleus muscle using microarray technology.

2017-01-20 | GSE93838 | GEO

Global gene expression analysis highlights microgravity sensitive key genes in soleus and EDL of 30 days space flown mice

Project description:Microgravity exposure as well as chronic muscle disuse are two of the main causes of physiological adaptive skeletal muscle atrophy in humans and murine animals in physiological condition. The aim of this study was to investigate, at both morphological and global gene expression level, skeletal muscle adaptation to microgravity in mouse soleus and extensor digitorum longus (EDL). Adult male mice C57BL/N6 were flown aboard the BION-M1 biosatellite for 30 days on orbit (BF) or housed in a replicate flight habitat on Earth (BG) as reference flight control. In this study, we investigated for the first time gene expression adaptation to 30 days of microgravity exposure in mouse soleus and EDL, highlighting potential new targets for improvement of countermeasures able to ameliorate or even prevent microgravity-induced atrophy in future spaceflights.

2017-01-15 | GSE80223 | GEO

miRNAs expression of soleus response to simulated microgravity

Project description:Identification of gravisensitive miRNAs expression in rat soleus muscle exposed to 7 and 14 days of Hindlimb suspension (HS) simulated microgravity. Microgravity causes muscle atrophy possibly due to muscle wasting overtake regeneration. Results provide insight into the molecular mechanisms regulating muscle atrophy. The expression of 23 out of 174 miRNAs was found to change at least 2-fold of 7 and/or 14 days of TS. By using real-time PCR assays, we verified the microarray data using some of the expected genes. The tissue was collected from Sprague-Dawley rats (8 weeks of age) subjected to 7, 14days of TS. miRNA expression profile was determined in three groups: control (CN), TS for 7 days (TS-7), and TS for 14 days (TS-14).Three miRNA microarray chips were analyzed for mixture of four samples of each of the three groups.

2013-11-05 | E-GEOD-52055 | biostudies-arrayexpress

Mouse muscle LC-MSMS upon weightlessness

Project description:Upon weightlessness and microgravity, deleterious effects on the neurosensory and neurovestibular systems, haematological changes, and deconditioning of musculoskeletal, cardiovascular and cardiopulmonary functions have been reported. In particular, loss of muscle mass and strength are triggered by weightlessness in humans during space flights, what is similarly observed as a result of physical inactivity conditions and ageing on Earth. However, skeletal muscle tissue is of paramount importance for health maintenance (e.g. being essential to locomotion, heat production, and metabolism). To better prevent or eventually treat microgravity-induced muscle atrophy, its underlying mechanisms have first to be characterized in details. Using cutting-edge quantitative proteomics, the aim of the present study was therefore to get an in depth view of the molecular regulations triggered by space conditions in skeletal muscles of mice during the 30-day flight of the BION-M1 biosatellite. As muscles differing in their fiber type composition appear to respond differently to microgravity (see above), we characterized here the differential response of the soleus, extensor digitorum longus and vastus lateralis muscles.

2017-06-14 | PXD005035 | Pride

Biological sex divergence in transcriptomic profiles during the onset of hindlimb unloading-induced atrophy

Project description:Disuse-induced muscle atrophy is a common clinical problem observed mainly in older adults, intensive care units patients, or astronauts. Previous studies presented biological sex divergence in progression of disuse-induced atrophy along with differential changes in molecular mechanisms possibly underlying muscle atrophy. The aim of this study was to perform transcriptomic profiling of male and female mice during the onset and progression of unloading disuse-induced atrophy. Male and female mice underwent hindlimb unloading (HU) for 24, 48, 72 and 168h (n=8/group). Muscles were weighed for each cohort and gastrocnemius was used for RNA-sequencing analysis. Females exhibited muscle loss as early as 24h of HU, while males after 168h of HU. In males, pathways related to proteasome degradation were upregulated throughout 168-h HU, while in females these pathways were upregulated up to 72-h HU. Lcn2, a gene contributing to regulation of myogenesis, was upregulated by 6.46–19.86-fold across all time points in females only. A reverse expression of Fosb, a gene related to muscle degeneration, was observed between males (4.27-fold up) and females (4.57-fold down) at 24-h HU. Mitochondrial pathways related to TCA cycle were highly downregulated at 168h of HU in males, while in females this downregulation was less pronounced. Collagen-related pathways were consistently downregulated throughout 168-h HU only in females, suggesting a potential biological sex-specific protective mechanism against disuse-induced fibrosis. In conclusion, females may have protection against HU-induced skeletal muscle mitochondrial degeneration and fibrosis through transcriptional mechanisms, although they may be more vulnerable to HU-induced muscle wasting compared to males.

2023-09-21 | GSE240814 | GEO

Delayed denervation-induced muscle atrophy in Opg knockout mice

Project description:Recent evidence has shown a crucial role for the osteoprotegerin/receptor activator of nuclear factor κ-B ligand/RANK (OPG/RANKL/RANK) signaling axis not only in bone but also in muscle tissue; however, there is still a lack of understanding of its effects on muscle atrophy. Here, we found that denervated Opg knockout mice displayed better functional recovery and delayed muscle atrophy, especially in a specific type IIB fiber. Moreover, OPG deficiency promoted milder activation of the ubiquitin-proteasome pathway, which further verified the protective role of Opg knockout in denervated muscle damage. Furthermore, transcriptome sequencing indicated that Opg knockout upregulated the expression of Inpp5k, Rbm3, and Tet2 and downregulated that of Deptor in denervated muscle. In vitro experiments revealed that satellite cells derived from Opg knockout mice displayed a better differentiation ability than those acquired from wild-type littermates. Higher expression levels of Tet2 were also observed in satellite cells derived from Opg knockout mice, which provided a mechanistic basis for the protective effects of Opg knockout on muscle atrophy. Taken together, our findings uncover the novel role of Opg in muscle atrophy process and extend the current understanding in the OPG/RANKL/RANK signaling axis.

2023-05-01 | GSE220152 | GEO

Genome-wide microarray analysis to identify the differentially expressed patterns of lncRNAs of cholesteatoma tissues compared with matched normal skin tissues.

Project description:We performed genome-wide microarray analysis to identify the differentially expressed patterns of lncRNAs in cholesteatoma. Our data indicated that lncRNA expression profiles were significantly altered in cholesteatoma compared with normal skin tissues. A total of 787 lncRNAs were identified (fold change ≥2.0, P < 0.05), consisting of 181 upregulated and 606 downregulated lncRNAs.

2018-05-09 | GSE102673 | GEO

RNA-sequencing data for 923 enhancer deletion newborn mouse whole skin

Project description:We examined the RNA expression profiles of whole skin from newborn CRISPR-edited mice that have the 923 enhancer located within the Epidermial Differentiation Complex deleted. We examined two independent deletion lines, 923del and 923large, both homozygous mutants and heterozygotes, as well as wild type mice and involucrin Ivl knockout mice. We find that Ivl, the gene most proximal to 923, is downregulated upon the loss of the enhancer in both independent deletions, and 4 additional genes are also downregulated in both deletion lines, a secondary effect of the loss of Ivl, as concluded by comparing to the Ivl KO mice. We thus conclude that Ivl is the primary target gene of the 923 enhancer and establish a 923-Ivl regulatory module.

2020-10-30 | GSE158869 | GEO

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