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A comparison of bone microarchitectural and transcriptomic changes in murine long bones in response to hindlimb unloading and aging

ABSTRACT: A comparison of bone microarchitectural and transcriptomic changes in murine long bones in response to hindlimb unloading and aging

PROVIDER: PRJNA988065 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25040655_1.fastq.gz	Fastqsanger.gz
	SRR25040655_2.fastq.gz	Fastqsanger.gz
	SRR25040656_1.fastq.gz	Fastqsanger.gz
	SRR25040656_2.fastq.gz	Fastqsanger.gz
	SRR25040657_1.fastq.gz	Fastqsanger.gz

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A comparison of bone microarchitectural and transcriptomic changes in murine long bones in response to hindlimb unloading and aging

Project description:Age and disuse-related bone loss both result in decreases in bone mineral density, cortical thickness, and trabecular thickness and connectivity. Disuse induces physiological changes in bone similar to those seen with aging. Animal studies used 6, and 22-month-old C57BL/6J male and female mice that were hindlimb unloaded (HLU) for 3 weeks. Ingenuity pathway analysis (IPA) included 4-month-old male mice unloaded for 3 weeks and a publicly available dataset (GLDS647) from 3-month female C57BL/6N mice unloaded for 7 days. There were age- and sex-dependent changes in bone structure and mechanical properties in response to HLU. The cortical bone and epiphyseal trabecular bone compartments were most affected. There were greater changes in bone mechanical properties due to age in males, and HLU in females. RNA extracted from whole-bone marrow-flushed tibiae was sequenced and analyzed. Gene ontology analysis demonstrated that mitochondrial function was downregulated after HLU whereas cell-cycle transition was downregulated with aging. IPA was used to identify the leading canonical pathways and upstream regulators in each HLU age group. IPA identified “Senescence Pathway” as the third leading canonical pathway enriched in mice exposed to HLU. HLU induced activation of the senescence pathway in 3 month and 4-month-old mice, inhibited it in 6-month-old mice and did not change it in 22 month old mice. In conclusion, we demonstrate that hindlimb unloading initiates changes in bone microarchitecture and gene expression characteristic of aging, but with distinct differences.

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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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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.

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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.

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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:A recent physiological study established that hindlimb unloading of rats at 3 and 7 weeks inhibits healing of injured ligaments, resulting in a badly aligned, discontinuous collagen matrix. Using tissue from these rats, we focused on the 3-week time point employing microarray analysis to identify what cellular processes or lack of processes could account for these observed deficiencies. We used the Afyymetrix RG_U34A GeneChip and performed image analysis with Microarray Suite 5.0. For normalization we used the MAS global normalization protocol with a default target mean signal of 500. Gene expression in medial collateral ligament tissue under 4 different treatment conditions was measured: loaded control, loaded wound healing, unloaded control, and unloaded wound healing. From our results, it appears that unloaded tissue lags behind loaded tissue in its progression through the healing process and at 3 weeks is still engaged in the proliferative phase, whereas loaded tissue is actively remodeling its collagen matrix. Summary tables below: Affymetrix MAS comparative analysis data for the 1778 genes qualified for further analysis as a result of detection call values. Keywords: other

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Skeletal muscle unloading affects muscle progenitor cells functional activity

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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Calycosin prevents bone loss induced by hindlimb unloading.

Project description:Bone loss induced by microgravity exposure seriously endangers the astronauts' health, but its countermeasures still have certain limitations. The study aims to find potential protective drugs for the prevention of the microgravity-induced bone loss. Here, we utilized the network pharmacology approach to discover a natural compound calycosin by constructing the compound-target interaction network and analyzing the topological characteristics of the network. Furthermore, the hind limb unloading (HLU) rats' model was conducted to investigate the potential effects of calycosin in the prevention of bone loss induced by microgravity. The results indicated that calycosin treatment group significantly increased the bone mineral density (BMD), ameliorated the microstructure of femoral trabecular bone, the thickness of cortical bone and the biomechanical properties of the bone in rats, compared that in the HLU group. The analysis of bone turnover markers in serum showed that both the bone formation markers and bone resorption markers decreased after calycosin treatment. Moreover, we found that bone remodeling-related cytokines in serum including IFN-γ, IL-6, IL-8, IL-12, IL-4, IL-10 and TNF-α were partly recovered after calycosin treatment compared with HLU group. In conclusion, calycosin partly recovered hind limb unloading-induced bone loss through the regulation of bone remodeling. These results provided the evidence that calycosin might play an important role in maintaining bone mass in HLU rats, indicating its promising application in the treatment of bone loss induced by microgravity.

| S-EPMC9259590 | biostudies-literature

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