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Basal gene expression in bone

ABSTRACT: Analysis of basal gene expression of the protective bones of the skull (parietals) and weight-bearing bones of the limb (ulnae)

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE12966 | GEO | 2008/11/15

SECONDARY ACCESSION(S): PRJNA114255

REPOSITORIES: GEO

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Pilot study: Basal gene expression in bone

Project description:Pilot study Analysis of basal gene expression of the protective bones of the skull (parietals), weight-bearing bones of the limb (ulnae) and mandibular bone and teeth

2008-11-15 | GSE13563 | GEO

Transcription profiling of mouse protective bones of the skull (parietals), weight-bearing bones of the limb (ulnae), mandibular bone and teeth to obtain basal gene expression levels

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Transcription profiling of protective bones of the skull (parietals) and weight-bearing bones of the limb (ulnae) in rats to obtain basal gene expression levels

Project description:Analysis of basal gene expression of the protective bones of the skull (parietals) and weight-bearing bones of the limb (ulnae) Experiment Overall Design: RNA extraction from normal bone

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Characterization of distinct classes of differential gene expression in osteoblast cultures from non-syndromic craniosynostosis bone

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Multi-omics and 3D-imaging reveal bone heterogeneity and unique calvaria cells in neuroinflammation

Project description:The bone marrow in the skull is important for shaping immune responses in the brain and meninges, but its molecular makeup in comparison to other bones in mice and humans remains unclear. Here, we show that the skull has the most distinct transcriptomic profile compared to other bones in states of health and injury, characterized by a late-stage neutrophil phenotype. In humans, proteome analysis reveal that the skull marrow is the most distinct, with differentially expressed neutrophil-related pathways and a unique synaptic protein signature. 3D imaging demonstrates the structural and cellular details of human skull-meninges connections compared to veins. Lastly, using TSPO-PET imaging, we show that the skull bone marrow reflects inflammatory brain responses with a disease-specific spatial distribution in patients with various neurological disorders. The unique molecular profile, anatomical, and functional connections of the skull show its potential as a new site for diagnosing, monitoring, and treating brain diseases.

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Multi-omics and 3D-imaging reveal bone heterogeneity and unique calvaria cells in in mice and humans

Project description:The meninges of the brain are an important component of neuroinflammatory response. Diverse immune cells move from the calvaria marrow into the dura mater via recently discovered skull-meninges connections (SMCs). However, how the calvaria bone marrow is different from the other bones and whether and how it contributes to human diseases remain unknown. Using multi-omics approaches and whole mouse transparency we reveal that bone marrow cells are highly heterogeneous across the mouse body. The mouse calvaria and the human skull harbors the most distinct molecular signature with hundreds of differentially expressed genes and proteins when compared to other bones. Our study indicates that the calvaria is more than a physical barrier, and its immune cells may present new ways to control brain pathologies.

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Project description:Diverse immune cells move from the calvaria marrow into the dura mater via recently discovered skull-meninges connections (SMCs). Yet, how the calvaria bone marrow is different from the other bones and whether it plays a special role in human diseases remain unknown. Using multi-omics approaches and whole mouse transparency we reveal that bone marrow cells are highly heterogeneous across the mouse body. The calvaria harbors the most distinct molecular signature with hundreds of differentially expressed genes and proteins. Acute brain injury induces skull-specific outcomes including increased calvaria cell numbers. Moreover, TSPO-PET imaging of stroke, dementia and multiple sclerosis patients demonstrate increased inflammation in the human skull, mirroring the underlying brain inflammation.

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The prenatal frontal and parietal bones are distinct organs.

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Project description:Osteoblasts require substantial amounts of energy to synthesize bone matrix and coordinate the mineralization of the skeleton. This study analyzed the effect of mitochondrial dysfunction on bone formation in mouse limbs. The limb mesenchyme-specific Tfam knockout (Tfamf/f;Prx1-Cre: Tfam-cKO) mice were analyzed morphologically, and histologically and gene expression in the limb bones were assessed by in situ hybridization, quantitative real-time PCR and RNA sequencing. Moreover, we analyzed mitochondrial function of osteoblasts in Tfam-cKO mice by mitochondrial membrane potential assay and transmission electron microscopic (TEM) observations. We investigated the pathogenesis of spontaneous bone fractures by immunohistochemical analysis, TEM observations and biomechanical examination. The forelimbs in Tfam-cKO mice were significantly shortened from birth and occurred spontaneous fractures within the first week after birth, resulting in severe limb deformities. Histologically, bone hypoplasia with decrease of matrix mineralization was apparent, and the expressions of type Ⅰ collagen and osteocalcin were decreased in the osteoblasts of Tfam-cKO mice although Runx2 expression was unchanged. Decreased type Ⅰ collagen deposition and mineralization in the matrix of the limb bones in Tfam-cKO mice was associated with marked mitochondrial dysfunction. Biomechanical analysis showed significantly lower Young’s modulus and hardness due to poor apatite orientation in the bone tissue of Tfam-cKO mice. The mice with limb mesenchyme-specific Tfam deletion exhibited spontaneous limb bone fractures, resulting in severe limb deformities. Their bone fragility was caused by poor apatite orientation due to impaired osteoblasts differentiation and maturation.

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Differentially expressed genes during disuse atrophy.

Project description:To identify atrophy genes directly targeted by Bcl-3 transactivator at a genome wide level, we performed whole transcript expression array and ChIP-seq for muscles from weight bearing or 5-day hind limb unloaded mice. Genes that showed increased expression with unloading and a Bcl-3 peak in the promoter (from ChIP-seq data) were considered as Bcl-3 direct targets during disuse atrophy. Using ChIP array, we identified 241 direct targets for Bcl-3. Our data describe Bcl-3 as a global regulator both of the proteolysis and the change in energy metabolism that are essential components of muscle atrophy due to disuse. Disuse skeletal muscle atrophy was induced by hind limb unloading. Weight bearing (WB) or 5-day hind limb unloaded (HU) muscles were harvested for total RNA isolation and processed for whole transcript expression profiling. We chose to examine gene expression and Bcl-3 binding from 5-day unloaded muscles because our previous time course study of disuse atrophy suggested that most genes are differentially regulated at this time point, and thus, would best represent the time for Bcl-3 binding to the gene targets of the NF-kB transcriptional network.

2012-11-10 | E-GEOD-40578 | biostudies-arrayexpress

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