Global analysis of microRNA target sites in human osteoblasts
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE111432 | GEO | 2018/09/05
REPOSITORIES: GEO
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Project description:Global analysis of microRNA target sites in human osteoblasts
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Project description:We report the application of RNA immunoprecipitation sequencing technology to identify targets of RNA-binding protein, Samd4, in osteoblasts. By obtaining sequences from immunoprecipitated RNA, we generated several mRNAs which could be bound by Samd4 in mouse osteoblasts.
2016-12-03 | GSE90818 | 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: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:Although Dicer1 functions as a haploinsufficient tumour suppressor its complete loss of function is selected against during tumourigenesis. Here we show that homozygous loss of Dicer1 prevents retinoblastoma formation in mice by synthetic lethality with combined inactivation of the p53 and Rb tumor suppressor pathways. We show that Dicer1 deficiency is tolerated in Rb-deficient retinal progenitor cells harbouring an intact p53 pathway, but not in absence of p53. The synthetic lethal interaction is mediated by the oncogenic miR-17?92 cluster since its deletion phenocopies Dicer1 loss in this context. Accordingly, miR-17?92- inactivation suppresses retinoblastoma formation in mice and co-silencing of miR17/20a and p53 cooperatively decrease the viability of pre-formed human retinoblastoma cells. These data provide important insights into what underlies selective pressure against loss of Dicer1 during tumorigenesis and indicate that targeting Dicer or miR-17-20a family members should be explored as a potential selective therapeutic approach for retinoblastoma prevention and/or treatment. 23 murine samples
2012-07-05 | E-GEOD-39106 | biostudies-arrayexpress
Project description:Although Dicer1 functions as a haploinsufficient tumour suppressor its complete loss of function is selected against during tumourigenesis. Here we show that homozygous loss of Dicer1 prevents retinoblastoma formation in mice by synthetic lethality with combined inactivation of the p53 and Rb tumor suppressor pathways. We show that Dicer1 deficiency is tolerated in Rb-deficient retinal progenitor cells harbouring an intact p53 pathway, but not in absence of p53. The synthetic lethal interaction is mediated by the oncogenic miR-17∼92 cluster since its deletion phenocopies Dicer1 loss in this context. Accordingly, miR-17∼92- inactivation suppresses retinoblastoma formation in mice and co-silencing of miR17/20a and p53 cooperatively decrease the viability of pre-formed human retinoblastoma cells. These data provide important insights into what underlies selective pressure against loss of Dicer1 during tumorigenesis and indicate that targeting Dicer or miR-17-20a family members should be explored as a potential selective therapeutic approach for retinoblastoma prevention and/or treatment. 36 human samples
2012-07-05 | E-GEOD-39105 | biostudies-arrayexpress
Project description:Mice with conditionally deactivating mutations in Mycn (Mycnfl/fl) or mir17-92 & mir106b (mir17-92fl/fl ; mir106b-/-) were crossed with mice expressing Cre-recombinase driven by the Prx1 promoter (Prx1Cre). Embryos were collected at E10.5, and distal compartment of hind- and fore-limbs were isolated from wild-type and conditional knock-out embryos (n=3 replicates per biologic group). Total RNA was extracted from each specimen with Trizol, and used in RNA-seq library preparation with Illumina Truseq mRNA library kit. Libraries were sequenced on the Illumina NextSeq system with 75bp single end reads.
2017-05-24 | E-MTAB-5671 | biostudies-arrayexpress
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 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