Bone Microarchitecture
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA671151 | ENA |
REPOSITORIES: ENA
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Project description:Early life resource limitation is one factor that could have a major impact on child health and development. Thus, using a rat model of limited bedding and nesting (LBN), we investigated the postnatal bone development, mineralization, and microarchitecture. Pregnant Sprague-Dawley rats were subjected to a LBN model to induce chronic early life stress (CES), while a control group was maintained under standard conditions. The offspring were assessed at postnatal day (PND) 10, 21, and 35. Tibial length was measured, and tibial and lumbar vertebral bone mineral density (BMD), content (BMC), and area (BMA) were assessed using dual-energy X-ray absorptiometry (DXA). Bone microarchitecture was examined using microcomputed tomography (μCT). Changes in gene expression from the lumbar vertebrae were analyzed by transcriptome. At PND 10, there were no significant differences in BMD and BMC between the treatment groups, but tibial length was significantly decreased by CES. By PND 21, tibial BMC and BMA were significantly reduced in the CES group, indicating impaired bone mineral accumulation. At PND 35, tibial length remained significantly reduced by CES, while BMD and BMC differences were less affected. Vertebral BMA and BMC were reduced by CES. μCT analysis of tibial cortical bone showed significant changes in cortical thickness and bone volume at PND 10 and 21, respectively. For the lumbar vertebrae, μCT data indicated significant increases in the degree of anisotropy and structural model index at PND 21 and 35, respectively. Transcriptome analyses revealed significant differential expression of genes involved in immune response, cellular repair, and stress adaptation at PND 21 but not at PND 10 and PND 35. CES significantly disrupts BMC, BMD, length and microarchitecture differently at various stages of postnatal development. Transcriptome analyses suggest that these changes are mediated by alterations in gene expression related to immune function and cellular repair. Future research should focus on tracking the longitudinal impacts of CES on bone health from infancy into adulthood, and exploring nutritional interventions, stress reduction programs, and molecular studies that can mitigate the negative effects of CES on bone.
2025-05-19 | GSE297538 | GEO
Project description:Osteoporosis is a metabolic disease characterized by the destruction of bone microarchitecture and bone loss, which increases the risk of fractures and reduces quality of life. Understanding the biological mechanisms that promote bone formation is therefore of great importance. In this study, we performed transcriptomic sequencing to molecularly elucidate the effects of Ilex paraguariensis extracts on bone formation and bone-related health. Thus, this study identifies the potential mechanisms by which Ilex paraguariensis and Ligularia fischeri extracts influence bone formation and the bone microenvironment and suggests potential targets and benchmarks for biological research.
2025-07-07 | GSE301490 | GEO
Project description:Obesity has emerged as a worldwide problem in human health. Dietary lipids are taken up and transported via lymphatics into the circulatory system. During this process, lipids pass the mesenteric lymph node (mLN). These organs filter the lymph fluid for foreign antigens to induce and control immune responses. Alteration of that function during obesity has only slightly been studied. Here, we characterize changes within the microarchitecture of the mLN during high levels of lipid transport and highlight the role of stromal cells. Microarray experiments detected gene probes expressed by mLN stromal cells. Transmission electron microscopy enabled us to identify lipid droplets in different stromal cells, and in macrophages. Sizes, numbers and intercellular distances increased after 10 weeks of a high-fat diet. Thus, we propose that changes in the microarchitecture and increased accumulation of lipid droplets in stromal cells and macrophages have an influence on the immunological function of the mLN.
2020-05-14 | GSE138593 | GEO
Project description:Obesity has emerged as a worldwide problem in human health. Dietary lipids are taken up and transported via lymphatics into the circulatory system. During this process, lipids pass the mesenteric lymph node (mLN). These organs filter the lymph fluid for foreign antigens to induce and control immune responses. Alteration of that function during obesity has only slightly been studied. Here, we characterize changes within the microarchitecture of the mLN during high levels of lipid transport and highlight the role of stromal cells. Microarray experiments detected gene probes expressed by mLN stromal cells. Transmission electron microscopy enabled us to identify lipid droplets in different stromal cells, and in macrophages. Sizes, numbers and intercellular distances increased after 10 weeks of a high-fat diet. Thus, we propose that changes in the microarchitecture and increased accumulation of lipid droplets in stromal cells and macrophages have an influence on the immunological function of the mLN.
2020-05-14 | GSE138594 | GEO
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Project description:<p>Osteoporosis is a metabolic bone disorder characterized by aberrant osteoclast activation, leading </p><p>to excessive bone resorption and microarchitectural deterioration. Although the interconnection </p><p>between osteoclast differentiation and cellular energy metabolism has been increasingly appreciated, </p><p>the contribution of pyrimidine metabolism to this process remains largely undefined. Here, </p><p>integrative transcriptomic and metabolomic profiling delineated a distinct metabolic remodeling </p><p>during osteoclastogenesis and identified uridine as a pivotal metabolite exhibiting a pronounced </p><p>decline upon RANKL stimulation. Functional and mechanistic studies demonstrated that exogenous </p><p>uridine supplementation effectively restrained osteoclast formation and bone resorptive activity, </p><p>concomitant with the downregulation of NFATc1 and CTSK expression. In OVX mice, uridine </p><p>administration ameliorated trabecular microarchitecture, reduced osteoclast burden, and mitigated </p><p>bone loss. Mechanistically, uridine inhibited PI3K/Akt phosphorylation, facilitated FoxO nuclear </p><p>translocation, and suppressed ROS accumulation, thereby preventing NFATc1 activation and </p><p>nuclear import. Collectively, this study uncovers a previously uncharacterized metabolic–signaling </p><p>coupling mechanism linking pyrimidine metabolism to osteoclastogenesis and establishes uridine </p><p>as a potential metabolic modulator for the prevention and treatment of osteoporosis. </p>
2026-04-09 | MTBLS13394 | MetaboLights
Project description: Not available
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