Expression data from c-Src inhibited osteoblasts
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE34570 | GEO | 2013/12/20
SECONDARY ACCESSION(S): PRJNA151013
REPOSITORIES: GEO
Similar Datasets
Project description:The tyrosine kinase c-Src has a crucial role in maintaining osteoblast in a less differentiated status, as already described in the literature. We used microarrays to detail the global programme of gene expression in osteoblasts treated with a well known c-Src inhibitor (PP1). Osteoblast primary cultures were isolated from calvaria of 7 days-old CD1 mice. These cell were starved and treated with vehicle (DMSO) or 2 micromolar PP1 for 24 hours. Then RNA was extracted and hybridizated on Affymetrix microarray.
2013-12-20 | E-GEOD-34570 | biostudies-arrayexpress
Project description:Osteoarthritis (OA) is the most common joint disease and this is a major cause of joint pain and disability in the aging population. Its etiology is multifactorial (i.e., age, obesity, joint injury, genetic predisposition), and the pathophysiologic process affects the entirety of the joint (Martel-Pelletier J et al. Osteoarthritis. Nature reviews Disease primers. 2016;2:16072). Although it is not yet clear if it precedes or occurs subsequently to cartilage damage, subchondral bone sclerosis is an important feature in OA pathophysiology (Goldring SR et al. Changes in the osteochondral unit during osteoarthritis: structure, function and cartilage-bone crosstalk. Nat Rev Rheumatol. 2016;12:632-44). It is characterized by local bone resorption and the accumulation of weakly mineralized osteoid substance (Bailey AJ et al. Phenotypic expression of osteoblast collagen in osteoarthritic bone: production of type I homotrimer. Int J Biochem Cell Biol. 2002;34:176-82). Subchondral bone sclerosis is suspected to be linked to cartilage degradation, not only by modifying the mechanical stresses transmitted to the cartilage, but also by releasing biochemical factors with an activity on cartilage metabolism (Sanchez C et al. Osteoblasts from the sclerotic subchondral bone downregulate aggrecan but upregulate metalloproteinases expression by chondrocytes. This effect is mimicked by interleukin-6, -1beta and oncostatin M pre-treated non-sclerotic osteoblasts. Osteoarthritis Cartilage. 2005;13:979-87; Sanchez C et al. Subchondral bone osteoblasts induce phenotypic changes in human osteoarthritic chondrocytes. Osteoarthritis Cartilage. 2005;13:988-97; Westacott CI et al J. Alteration of cartilage metabolism by cells from osteoarthritic bone. Arthritis Rheum. 1997;40:1282-91. We have previously demonstrated that osteoblasts isolated from subchondral OA bone exhibited an altered phenotype. More precisely, we showed that osteoblasts coming from the thickening (called sclerotic, SC) of subchondral bone located just below a cartilage lesion produced higher levels of alkaline phosphatase, interleukin (IL)-6, IL-8, prostaglandinE2, vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-9 and transforming growth factor(TGF)-β1 and type I collagen than osteoblasts coming from the non-thickening neighboring area (called non-sclerotic area, NSC) (Sanchez C et al. Phenotypic characterization of osteoblasts from the sclerotic zones of osteoarthritic subchondral bone. Arthritis Rheum. 2008;58:442-55; Sanchez C et al. Regulation of subchondral bone osteoblast metabolism by cyclic compression. Arthritis Rheum. 2012;64:1193-203.) To compare secretome of cells living in different in vivo conditions is useful, not only to better understand the pathological mechanisms underlying changes in OA subchondral bone, but also to identify soluble biomarkers potentially reflecting these changes. Using our well-characterised human subchondral osteoblast culture model, we compared the secretome of osteoblasts coming from sclerotic and non sclerotic OA subchondral bone. This approach allowed to identify changes in secretome that contribute to explain some subchondral bone abnormalities in OA and to propose osteomodulin and fibulin-3 as potential biomarkers of OA subchondral bone remodelling.
2018-03-20 | PXD008494 | Pride
Project description:Osteoblasts are a key component of the endosteal hematopoietic stem cell (HSC) niche and have long been recognized with strong hematopoietic supporting activity. Osteoblast conditioned media (OCM) enhances the growth of hematopoietic progenitors in culture and modulate their engraftment activity. We aimed to characterize the hematopoietic supporting activity of OCM by comparing the secretome of immature osteoblasts to that of their precursor, mesenchymal stromal cells (MSC). Over 300 secreted proteins were quantified by mass spectroscopy in media conditioned with MSC or osteoblasts, with 47 being differentially expressed.
2020-07-17 | PXD017372 | Pride
Project description:Here, we used single-cell RNA sequencing (scRNA-seq) to provide a high-resolution cellular taxonomy of freshly isolated primary human osteoblasts. Based on the gene expression patterns and cell lineage reconstruction, we identified three distinct clusters including preosteoblasts, mature osteoblasts, and an undetermined rare osteoblast subpopulation. Trajectory inference analysis suggested that the undetermined cluster may include osteoblast precursor cells which regulate the osteoblastogenesis process by giving rise to pre and mature osteoblasts. Investigation of the biological processes and signaling pathways enriched in each subpopulation revealed that in addition to bone formation, pre and undetermined osteoblasts may regulate both angiogenesis and hemopoiesis.
2021-03-01 | GSE147390 | GEO
Project description:Osteoblasts are a key component of the endosteal hematopoietic stem cell (HSC) niche and have long been recognized with strong hematopoietic supporting activity. Osteoblast conditioned media (OCM) enhances the growth of hematopoietic progenitors in culture and modulate their engraftment activity. We aimed to characterize the hematopoietic supporting activity of OCM by comparing the secretome of immature osteoblasts to that of their precursor, mesenchymal stromal cells (MSC). Over 300 secreted proteins were quantified by mass spectroscopy in media conditioned with MSC or osteoblasts, with 47 being differentially expressed.
2021-11-15 | MSV000088384 | MassIVE
Project description:Osteoblasts are adherent cells. Under physiological conditions they attach to mineralized and non-mineralized osseous surfaces. However, how exactly osteoblasts respond to these different osseous surfaces is largely unknown. Our hypothesis was that the state of matrix mineralization provides a functional signal to osteoblasts. To assess the osteoblast response to mineralized compared to demineralized osseous surfaces, we assessed the transcriptom.
2018-09-30 | GSE114237 | GEO
Project description:We utilized RNA sequencing to provide the gene expression profile of mesenchymal stem cells (MSCs) derived osteoblasts in different differentiation stages as well as the gene alteration profile of H9 MSCs-derived osteoblasts following different gene regulation treatments, including SDC1 overexpression, knockout of CEBPD, knockout of IL1R1, and knockdown of CORIN. The commitment of stem cells to an osteoblastic lineage is a complex and tightly regulated process, involving coordination between extrinsic signals and intrinsic transcriptional machinery. While many rodent osteoblast studies abound, human osteoblastic signaling networks are not as well-researched due to limitations in cell sources and existing models. Here, we generated human pluripotent stem cell (hPSC)-derived osteoblasts and used this modeling platform to identify functional osteoblastic surface receptors and their downstream transcriptional networks involved in human osteogenesis. We systematically dissected osteoblastic gene expression patterns and identified critical clusters associated with osteogenesis. The osteoblast surface receptor signature study revealed enriched CORIN expression in osteoblasts and enriched SDC1 expression in MSCs. In vitro calcified staining and 3D biomimetic GelMA/microCT (μCT) studies demonstrated that depletion of CORIN as well as ectopic expression of SDC1 significantly impaired osteogenesis. Transcriptome analyses revealed that dysregulation of CORIN or SDC1 alters biological processes and pathways mainly involved in bone formation associated signaling including TGFβ regulating extracellular matrix and Wnt signaling. Genome-wide ChIP enrichment analysis further indicated that CEBPD is a downstream transcription factor involved in CORIN and SDC1-modulated osteogenesis. CEBPD ChIP-seq and RNA-seq validated its role in controlling extracellular matrix organization, bone mineralization, and TGFβ, BMP, and Wnt signaling. Depletion of CEBPD led to impairment of osteoblastic differentiation. Differential expression analysis of single-cell transcriptomes revealed enriched expression of CEBPD and its transcriptional targets during the different stages of osteoblast differentiation. In summary, our findings elucidated the vital signaling in osteoblast lineage commitment.
2023-04-28 | GSE202080 | GEO
Project description:We differentiated mouse Col2.3 GFP ESCs and iPSCs to osteoblast progenitors and confirmed the osteoblast identity of ESC- and iPSC-derived osteoblasts using RNA-sequencing and hierarchical clustering, and demonstrate that Col2.3GFP+ sorted cells are more similar to freshly isolated Col2.3GFP+ osteoblasts from mouse bone than to unsorted cells based on whole genome expression profiling.
2018-05-01 | GSE110434 | GEO
Project description:Bone is the most common site of breast cancer metastasis, and this type of metastasis is a main cause of morbidity. Because breast cancer is a heterogeneous disease, the interactions between the cancer cells and the skeletal host cells, such as osteoblasts, might be diverse. Thus far, these tumor-osteoblast interactions have not yet been well characterized using a genomic approach. We hypothesized that gene expression signatures induced by tumor-osteoblast interactions might be of clinical relevance. To examine these gene expression signatures, we established an ex vivo co-culture model with benign human cells and a panel of 5 malignant breast epithelial cells in combination with primary human osteoblasts and determined associated gene expression changes using cDNA microarrays. This SuperSeries is composed of the following subset Series: GSE29030: Normal human osteoblasts and HMEC mono and coculture GSE29031: Normal human osteoblasts and Hs578t mono and coculture GSE29032: Normal human osteoblasts and MCF7 mono and coculture GSE29033: Normal human osteoblasts and MDA-MB-231 mono and coculture GSE29034: Normal human osteoblasts and SKBR3 mono and coculture GSE29035: Normal human osteoblasts and T47D mono and coculture Refer to individual Series
2012-01-06 | E-GEOD-29036 | biostudies-arrayexpress
Project description:Global energy balance in mammals is controlled by the actions of circulating hormones that coordinate fuel production and utilization in metabolically active tissues. Bone-derived osteocalcin, in its undercarboxylated, hormonal form, regulates fat deposition and is a potent insulin secretagogue. Here, we show that insulin receptor (IR) signaling in osteoblasts controls osteoblast development and osteocalcin expression by suppressing the Runx2 inhibitor Twist-2. Mice lacking IR in osteoblasts have low circulating undercarboxylated osteocalcin and reduced bone acquisition due to decreased bone formation and deficient numbers of osteoblasts. With age, these mice develop marked peripheral adiposity and hyperglycemia accompanied by severe glucose intolerance and insulin resistance. The metabolic abnormalities in these mice are improved by infusion of exogenous under-carboxylated osteocalcin. These results indicate the existence of a bone-pancreas endocrine loop through which insulin signaling in the osteoblast ensures osteoblast differentiation and stimulates osteocalcin production, which in turn regulates insulin sensitivity and pancreatic insulin secretion to control glucose homeostasis. We used microarrays to detail the global gene expression changes in response to insulin acting through insulin receptor in osteoblasts and identified distinct genes specifically involved in bone remodeling process. 4 groups and 3 time points (0h as a control, 6h, 12h, and 24h)
2010-05-27 | E-GEOD-21710 | biostudies-arrayexpress