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Transcriptome of bone marrow cells from mice with osteoporosis induced bu hindlimb unloading

ABSTRACT: In order to investigate whether the bone marrow environment of OP-HU mice could lead to the expansion of HSCs and myeloid-biased hematopoiesis, bulk RNA-seq of was performed with whole bone marrow cells of mice after hindlimb unloading

ORGANISM(S): Mus musculus

PROVIDER: GSE281210 | GEO | 2025/12/04

REPOSITORIES: GEO

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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.

2025-05-07 | PXD057671 | Pride

Transcriptome of bone marrow cells from mice with osteoporosis induced bu hindlimb unloading

Project description:Transcriptome of bone marrow cells from mice with osteoporosis induced bu hindlimb unloading

| PRJNA1182730 | ENA

Expression data from intestinal epithelial cells of hindlimb unloading (HU) and control mice

Project description:Commensal bacteria can manipulate the proliferation, differentiation, and survival of intestinal epithelial cells. Hindlimb unloading alters the composition and structure of the microbial community. To further characterize the epithelial changes, we performed a genome-wide microarray analysis of colon epithelium isolated from HU and control mice.

2022-10-20 | GSE89277 | GEO

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.

2024-01-26 | PXD042753 | 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

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).

2023-07-16 | GSE237099 | GEO

RNA-sequencing of skeletal stem cells (SSC) and mesenchymal stem cells (MSC) from hindlimb unloaded and reloaded mice

Project description:Disuse osteoporosis (DO) occurs in response to mechanical unloading of the skeleton and results in structural changes that compromise bone strength leading to increased fracture risk. Although skeletal stem cells (SSCs) are the main source of osteoblasts and adipocytes in adult bone marrow, whether DO impacts SSC function has not been established. Here, three-month-old male C57BL/6 mice were subjected to a hindlimb unloading (HU) model of disuse osteoporosis for 8 or 14 weeks by tail suspension. Control mice (ambulatory or AMB) were allowed normal use of their hindlimbs. An additional cohort underwent an 8-week recovery period after 8-weeks of unloading. Bone marrow-derived, LepR+ skeletal stem cells (SSCs) were isolated by FACS (n=3 or 4) and pooled prior to RNA isolation. Where indicated, cultured, immuno-depleted, bone marrow-derived mesenchymal stem cells (MSCs) were also collected (n=3) and pooled prior to RNA isolation. Generated libraries were subjected to NGS RNA-seq analysis on the Illumina NextSeq 500. These data delineate unique physiological adaptations to prolonged unloading, demonstrate that DO results in increased leptin expression and sympathetic signaling within the BM niche.

2021-12-01 | GSE156174 | GEO

Skeletal muscle specific AMPKalpha1/2 deletion during hindlimb unloading

Project description:The primary goal of this study was to determine the role of AMPKalpha during disuse atrophy. Skeletal muscle-specific tamoxifen-inducible AMPKlpha1/alpha2 double knockout (KO) mice were generated and KO was induced for 4 weeks. After 2 weeks of KO, mice were hindlimb unloaded (HU) for 2 weeks to induce atrophy or maintained ambulatory (AMB). We observed that AMPKalpha double KO impaired skeletal muscle transcriptional profiles that may have carried over with HU.

2023-12-09 | GSE240909 | GEO

Single cell analysis reveals the myeloid-biased hematopoiesis and leukemic evolution programs initiated by Brd4 in HSPCs of mice with disuse osteoporosis

Project description:To understand the molecular changes driving the myeloid-biased hematopoiesis and the potential of leukemia evolution by restricting the differentiation and apoptosis in HSPCs of OP-HU mice, single cell RNA sequencing was performed to analyze the transcriptional changes of Lin-/c-kit+ HSPCs from the femur and tibia of OP-HU and control mice.

2025-11-14 | GSE281970 | GEO

Transcriptomic profiling of cortical bone from hindlimb unloaded mice

Project description:The goal of this study was to perform RNA-sequencing of cortical bone isolated from 11-week-old female hindlimb unloaded and control mice. Mice were subjected to hindlimb unloading for 7 days, followed by RNA isolation of cortical bone. Cortical transcriptomic profiles were assessed with RNAseq.

2021-03-23 | GSE169292 | GEO

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