Identify molecules regulated by glucosylceramide synthase in mouse osteoblasts.
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ABSTRACT:
PROVIDER: PRJNA729440 | ENA |
REPOSITORIES: ENA
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Project description:To identify molecules regulated by glucosylceramide synthase in osteoblasts, we conducted microarray analysis using samles treated with the inhibitors of glucosylceramide synthase.
2021-08-30 | GSE174323 | GEO
Project description:To screen mRNAs specifically regulated by mTORC1, a global mRNA expression profile in calvarial osteoblasts (OBs) from mice with or without OB-specific Tsc1 knockout was developed using microarray. Wild type (WT) or OB-specific Tsc1 knockout (KO) mice were sacrificed, with calvarial osteoblasts harvested and subjected to total RNA extraction.
2015-11-07 | E-GEOD-74781 | biostudies-arrayexpress
Project description:To screen mRNAs specifically regulated by mTORC1, a global mRNA expression profile in calvarial osteoblasts (OBs) from mice with or without OB-specific Tsc1 knockout was developed using microarray.
2015-11-07 | GSE74781 | GEO
Project description:Identified a series of miRNAs transcriptionally regulated by vitamin D treatment within osteoblasts. Several miRNAs were validated in dose escalation experiments. Furthermore, downstream miRNA targets were appraised and found to regulate target message and protein levels. These findings were assessed in early and late passaged osteoblasts and found an age-dependent regulation of some miRNAs, while others were considered constituitiously expressed. Inhibitor studies of one key bone-related miRNA demonstrated the importance of this miRNA to regulate vitamin D-mediate osteoblastic differentiation during mineralizaition. Three independent sets of passage 8 primary human osteoblasts were either treated with vehicle (ethanol) or 1,25D3 (10nM) for 6 hours. Total RNA was collected using the miRNA Vana kit (ABI) and then quality assessed, and sent for miRNA array processesing.
2012-07-31 | E-GEOD-34144 | biostudies-arrayexpress
Project description:Identified a series of miRNAs transcriptionally regulated by vitamin D treatment within osteoblasts. Several miRNAs were validated in dose escalation experiments. Furthermore, downstream miRNA targets were appraised and found to regulate target message and protein levels. These findings were assessed in early and late passaged osteoblasts and found an age-dependent regulation of some miRNAs, while others were considered constituitiously expressed. Inhibitor studies of one key bone-related miRNA demonstrated the importance of this miRNA to regulate vitamin D-mediate osteoblastic differentiation during mineralizaition.
2012-08-01 | GSE34144 | 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:Expression profiling analysis to identify POH1-regulated genes
| PRJNA432039 | ENA
Project description:Bone remodeling is a tightly regulated process that engages degradation and biogenesis of the bone matrix. The process is controlled by two major cell types, bone forming cells-osteoblasts and bone-degrading cells-osteoclasts. We are interested in the bone-resorption mechanism mediated by osteoclasts and wish to identify glycosylation genes that are regulated during the formation of osteoclast cells and determine the function of glycosylation and glycan-binding proteins in the osteoclastogenesis.
2011-04-29 | GSE28937 | 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:Single cell hibernation cultures identify molecules dispensable for haematopoietic stem cell self-renewal
| PRJNA672062 | ENA