Genome wide effects of vitamin C on in bone and during osteogenesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA577623 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10278700_1.fastq.gz | Fastqsanger.gz | |||
| SRR10278700_2.fastq.gz | Fastqsanger.gz | |||
| SRR10278701_1.fastq.gz | Fastqsanger.gz | |||
| SRR10278701_2.fastq.gz | Fastqsanger.gz | |||
| SRR10278702_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 102 |
Similar Datasets
Project description:Epigenetic effects of vitamin C on bone and osteogenic differentiation by analyzed RNA-seq, hMeDIP-seq and ChIP-Seq analysis
2022-06-10 | GSE138854 | GEO
Project description:Angiogenesis is uncoupled from osteogenesis during calvarial bone regeneration
| PRJNA1091559 | ENA
Project description:Osteoclast differentiation and activation requires the presence of osteoblast-derived factors such as Macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-kappaB ligand (RANKL). RANKL is influenced by osteotropic hormones such as calcitriol 1,25(OH)2D3 (vitamin D).The aim of this study is to evaluate the combined effect of vitamin D and M-CSF on murine bone marrow and on murine spleen cell, to define when the inhibitory effect of vitamin D plus M-CSF is maximum and what are the mechanisms involved in this inhibition. When murine bone marrow cells were cultured with 10-8 M vitamin D and 60 ng/ml M-CSF, there was a significant decrease in osteoclasts formation (3.13±3.44),compared to bone marrow cells cultured with vitamin D alone (80.86 ±45.02; p<0.05). Even when the amount of M-CSF added to the bone marrow cell culture was 1 ng/ml there was a 40% decrease in osteoclasts formation. Since bone marrow contains also stromal cells, we eliminate their influence by culturing murine spleen cells with 10-8 M vitamin D, 60 ng/ml M-CSF and RANKL 20 ng/ml. There was a significant decrease in osteoclasts formation (41±14.14) compared to spleen cells cultured with M-CSF and RANKL (215.67±46.44); p<0.05). These data lead to hypothesize that vitamin D and M-CSF together exert an inhibitory effect on osteoclast differentiation and development. To define the cellular mechanism involved in this inhibition we analyzed gene array data of bone marrow cells cultured with vitamin D and compare them with the cells cultured with vitamin D and M-CSF. Activation Toll like receptors after addition of vitamin D plus M-CSF to bone marrow cells appears to be involved in the inhibition of osteoclast differentiation. Keywords: parallel sample
2004-08-31 | GSE1587 | GEO
Project description:Orthodontic tooth movement (OTM) is primarily driven by alveolar bone remodeling, wherein tension-induced osteogenesis plays a central role. Importin7 (IPO7) has been identified as a highly mechanoresponsive nuclear transport receptor (NTR). However, its role in regulating tension-induced osteogenesis during OTM and its underlying mechanism remains elusive. In the present study, cyclic tensile strain and a rat OTM model were used to investigate the role of IPO7. The results revealed that IPO7 was significantly expressed both in vitro and in vivo following exposure to mechanical stretch. Moreover, IPO7 knockdown inhibited tension-induced osteogenesis in BMSCs. Upon mechanical force stimulation, IPO7 translocated from the cytoplasm to the nucleus. Furthermore, immunoprecipitation (IP) coupled with mass spectrometry (MS) was performed and demonstrated that RUNX2 was one of the IPO7-interacting proteins related to osteogenesis. Although RUNX2 has been established to translocate to the nucleus to facilitate osteogenesis, whether it is IPO7 that regulate RUNX2 nuclear input during tension-induced osteogenesis remains to be determined. Then, the interaction between IPO7 and RUNX2 was further validated via co-immunoprecipitation (co-IP) and colocalization assays in BMSCs using immunofluorescence. Taken together, this study demonstrates that IPO7 promotes tension-induced osteogenesis by regulating the nucleoplasmic localization of RUNX2. Thus, targeting IPO7 may represent a prospective therapeutic strategy for enhancing alveolar bone remodeling and the efficacy of orthodontic treatment.
2025-10-06 | PXD061760 | Pride
Project description:Induction of osteogenesis by bone-targeted Notch activation
| PRJNA638902 | ENA
Project description:Bone development and repair depends on the differentiation of mesenchymal stem cells (MSCs) into osteoblasts. MSCs can be differentiated towards osteoblasts in vitro, making these cells a convenient tool for investigation of osteogenesis. Molecular characterization of this process is relevant for the application of MSCs in skeletal regenerative medicine, and for understanding the deregulation of osteogenesis in bone disease. Cellular differentiation is driven by highly regulated changes in gene expression, which at the level of transcription is associated with DNA binding of transcriptional regulators and local changes in chromatin landscape. By sequencing of RNA (RNA-Seq) and immunoprecipitated chromatin (ChIP-Seq) we have characterized gene expression, histone modification changes and DNA binding of the bone master regulator RUNX2 in osteogenic differentiation. Data from the RNA-Seq experiment has also been deposited at ArrayExpress under accession number E-MTAB-1829 (https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1829/).
2013-09-01 | E-MTAB-1828 | biostudies-arrayexpress
Project description:Bone development and repair depends on the differentiation of mesenchymal stem cells (MSCs) into osteoblasts. MSCs can be differentiated towards osteoblasts in vitro, making these cells a convenient tool for investigation of osteogenesis. Molecular characterization of this process is relevant for the application of MSCs in skeletal regenerative medicine, and for understanding the deregulation of osteogenesis in bone disease. Cellular differentiation is driven by highly regulated changes in gene expression, which at the level of transcription is associated with DNA binding of transcriptional regulators and local changes in chromatin landscape. By sequencing of RNA (RNA-Seq) and immunoprecipitated chromatin (ChIP-Seq) we have characterized gene expression, histone modification changes and DNA binding of the bone master regulator RUNX2 in osteogenic differentiation. Data from the RNA-Seq experiment has also been deposited at ArrayExpress under accession number E-MTAB-1829 (https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1829/).
2013-09-01 | E-MTAB-1829 | biostudies-arrayexpress
Project description:Skeletal deformities are typical clinical manifestations of autosomal dominant hyper-immunoglobulin E syndrome (AD-HIES), but the treatment is still limited. AD-HIES is mainly caused by dominant-negative mutations in signal transducer and activator of transcription 3 (STAT3). Clarifying the mechanisms by which STAT3 inactivation destructs bone metabolism is, therefore, important. Although, a few lines of data indicate osteoporosis induced by STAT3 inactivation may be related to increased osteoclast activity, here, we firstly report that deletion of Stat3 in osteoblasts, but not in osteoclasts, induced AD-HIES-like bone defects, including craniofacial malformation, osteoporosis, and spontaneous bone fracture in mice, and these defects were resulted from impaired osteogenesis induced by STAT3 inactivation in osteoblasts, but not increased osteoclast activity. Mechanistic analysis revealed a novel regulatory model in which STAT3 drove osteoblast differentiation via promoting distal-less homeobox 5 transcription in cooperation with MSX1. Furthermore, inducible deletion of Stat3 in osteoblasts also inhibited osteogenesis and induced bone loss in adult mice. Meaningfully, pharmacological inhibition of STAT3 induced bone loss, while activation of STAT3 partially prevent bone loss due to tail sus-pension. Taken together, STAT3 is critical for both modulating skeletal development and maintaining bone homeostasis, and inactivation of STAT3 in osteoblasts, but not in osteoclasts, induced AD-HIES-related skeletal deformities by impairing osteogenesis, providing new insights for their treatment.
2021-07-28 | GSE173711 | GEO
Project description:Declining bone mass is associated with aging and osteoporosis, a disease characterized by progressive weakening of the skeleton and increased fracture incidence. Growth and lifelong homeostasis of bone involve interactions between different cell types including vascular cells and mesenchymal stromal cells (MSCs). As these interactions involve Notch signaling, we have explored whether treatment with secreted Notch ligand proteins can enhance osteogenesis in adult mice. We show that a bone-targeting, high affinity version of the ligand Delta-like 4 (termed Dll4(E12)) induces bone formation without causing adverse effects in other organs, which are known to rely on intact Notch signaling interactions. Single cell analysis of stromal cells indicates that Dll4(E12) primarily acts via bone marrow MSCs and has comparably minor effects on osteoblast lineage cells, endothelial cells or chondrocytes. Based on this example, we propose that bone-targeted fusion proteins might be therapeutically useful and can avoid detrimental effects caused by systemic administration.
2022-01-23 | GSE152285 | GEO
Project description:Transcriptome expression of human bone marrow mesenchymal stem cell (hBMSCs) during osteogenesis
| PRJNA740003 | ENA