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Transcriptomic profiles of testis from hindlimb unloaded mice treated with 4-phenylbutyrate

ABSTRACT: Transcriptomic profiles of testis from hindlimb unloaded mice treated with 4-phenylbutyrate

PROVIDER: PRJNA843959 | ENA |

REPOSITORIES: ENA

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Transcriptomic profiles of testis from hindlimb unloaded mice treated with 4-phenylbutyrate

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Transcriptomic profiles of liver tissue from hindlimb unloaded mice treated with 4-phenylbutyrate

Project description:Bulk transcriptomic profiles of liver tissues from male, 18 weeks old c57Bl/6j mice, including ground-based controls, hindlimb-unloaded mice treated with vehicle, and hindlimb unloaded mice treated wit 4-phenylbutyrate (4-PBA)

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Transcriptomic profiles of gastrocnemius muscles from hindlimb unloaded mice treated with 4-phenylbutyrate

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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.

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Hindlimb unloading alters wound healing in ligaments

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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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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