Genome wide gene expression profiling demonstrated that mouse ESC and iPSC differentiated osteoblast progenitors resemble osteoblasts
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ABSTRACT:
PROVIDER: PRJNA433694 | ENA |
REPOSITORIES: ENA
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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: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:Our preliminary data shows that dietary ACNs increased osteoblast differentiation and function in human osteoblasts, as well as increased osteoblast differentiation and reduced bone resorption in transgenic medaka. In cultured human osteoblasts, ACNs and resveratrol enhanced growth, reduced apoptosis and increased the expression of HDACs and PGC-1, suggesting that ACNs alter epigenetic regulation and mitochondrial biogenesis
2023-08-08 | GSE200683 | GEO
Project description:Our preliminary data shows that dietary ACNs increased osteoblast differentiation and function in human osteoblasts, as well as increased osteoblast differentiation and reduced bone resorption in transgenic medaka. In cultured human osteoblasts, ACNs and resveratrol enhanced growth, reduced apoptosis and increased the expression of HDACs and PGC-1, suggesting that ACNs alter epigenetic regulation and mitochondrial biogenesis
2023-08-08 | GSE200682 | GEO
Project description:We identified four transcriptional factors, Runx2, Osx, Dlx5, and ATF4, that rapidly and efficiently reprogram mouse fibroblasts derived from 2.3 kb type I collagen promoter-driven green fluorescent protein (Col2.3GFP) transgenic mice into induced osteoblast cells (iOBs). The global transcriptome profiling validated that iOBs resemble primary osteoblasts. Genome-wide DNA methylation analysis demonstrates that within differentially methylated loci, the methylation status of iOBs more closely resembles primary osteoblasts than mouse fibroblasts. We further demonstrate that Col2.3GFP+ iOBs have transcriptome profiles similar to GFP+ cells derived from Col2.3GFP transgenic mouse bone chips.
2020-01-01 | GSE139907 | 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.
2020-07-17 | PXD017372 | Pride
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: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