Targeting adipocyte ESRRA promotes osteogenesis and vascular formation in adipocyte-rich bone marrow
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1046038 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26968342_1.fastq.gz | Fastqsanger.gz | |||
| SRR26968342_2.fastq.gz | Fastqsanger.gz | |||
| SRR26968343_1.fastq.gz | Fastqsanger.gz | |||
| SRR26968343_2.fastq.gz | Fastqsanger.gz | |||
| SRR26968344_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:Extensive bone marrow adipocytes (BMAds) accumulation occurring under diverse pathophysiological conditions leads to bone deterioration.Estrogen-related receptor α (ESRRA) is a key regulator responding to metabolic stress.To explore the transcriptional role of ESRRA in regulating BMAds autonomous genes，bulk RNA-seq transcriptome analysis was performed in adipocyte-specific ESRRA deficiency BMAds lineage cells at 7 days upon adipogenic induction.
2024-03-07 | GSE248799 | GEO
Project description:In order to select mRNA transcripts strongly enriched in murine white adipocytes versus brown adipocytes or stromal-vascular fraction, gene expression data of the adipocyte and stromal-vascular fractions of the interscapular brown, inguinal subcutaneous as well as visceral epididymal adipose tissue depots of young adult male C57BL/6 mice housed at constant 23°C ambient temperature were obtained. 18 samples: 3 different adipose tissues separated into stromal-vascular fraction and adipocytes, analyzed in biological triplicates.
2013-04-27 | E-GEOD-44059 | biostudies-arrayexpress
Project description:In order to select mRNA transcripts strongly enriched in murine white adipocytes versus brown adipocytes or stromal-vascular fraction, gene expression data of the adipocyte and stromal-vascular fractions of the interscapular brown, inguinal subcutaneous as well as visceral epididymal adipose tissue depots of young adult male C57BL/6 mice housed at constant 23°C ambient temperature were obtained.
2013-04-27 | GSE44059 | GEO
Project description:Products of adipocytes control bone cells and may therefore lead to new anti-osteoporosis therapies. To address this issue we mated mice expressing the primate diphtheria toxin receptor (DTR), which is equivalent to Heparin Binding Epidermal Like Growth Factor (HB-EGF), under control of a Stop-flox cassette, to those expressing adiponectin-Cre (ADQ-Cre). Injected diphtheria toxin (DT) completely eliminates white and brown adipose tissue in these DTRADQ mice and ablates marrow adipocytes. Medullary bone of DTRADQ mice begins to accumulate, due to stimulated osteoblast recruitment and differentiation, within 4 days of injected DT. By 10-14 days of DT administration to DTRADQ mice, trabecular bone has increased 1000%. Two months after fat ablation, cortical thickness has markedly increased as has bone strength. To gain insight into the signaling events by which DT/DTRADQ adipocyte ablation promotes osteogenesis we performed RNAseq analysis of marrow prior to and after 1-3 days of DT injection. This exercise confirms ablation of marrow adipocytes, as adiponectin expression is markedly reduced while enhanced expression of Col1a1 and Col1a2 genes is in keeping with stimulated osteogenesis. RNAseq analysis also indicates that DT/DTRADQ-induced osteogenesis is mediated by the BMPR pathway. For example, there is suppressed genetic expression of the specific BMPR inhibitors, chordin-like1 (CHRDL1) and gremlin1 (GREM1). This adipocyte ablation-mediated increase in bone mass is due to cooperative activation of BMP and EGF receptor signaling as adipocyte-produced inhibitors are suppressed and downstream targets activated or expressed. Medicinal inhibition of either signaling pathway prevents induction of the osteosclerotic phenotype. DTR-induced post-natal osteogenesis does not represent the products of peripheral fat depots and is more likely due to those of marrow adipocytes. Thus, anabolic drugs activating both BMP and EGF receptor signaling may be a means of profoundly increasing bone mass and treating osteoporosis.
2020-11-06 | GSE154800 | GEO
Project description:Age-induced decline in osteogenic potential of bone marrow mesenchymal stem cells (BMSCs) potentiates osteoporosis and increases risk for bone fractures. Despite epidemiology studies reporting concurrent development of vascular- and bone diseases in the elderly, the underlying mechanisms for the vascular-bone cross-talk in aging are largely unknown. In this study, we show that accelerated endothelial aging deteriorates bone tissue through paracrine repression of Wnt-driven-axis in BMSCs. Here, we utilize physiologically aged mice in conjunction with our transgenic endothelial progeria mouse model (Hutchinson-Gilford progeria syndrome; HGPS) that displays hallmarks of an aged bone marrow vascular niche. We find bone defects associated with diminished BMSC osteogenic differentiation that implicate the existence of angiocrine factors with long-term inhibitory effects. microRNA-transcriptomics of HGPS-patient plasma combined with aged-vascular niche analyses in progeria mice reveal abundant secretion of Wnt-repressive microRNA-31-5p. Moreover, we show that inhibition of microRNA-31-5p as well as selective Wnt-activator CHIR99021 boost the osteogenic potential of BMSCs through de-repression and activation of the Wnt-signalling, respectively. Our results demonstrate that the vascular niche significantly contributes to osteogenesis defects in aging and pave ground for microRNA-based therapies of bone loss in elderly.
2024-07-10 | GSE271848 | GEO
Project description:The expression of Glis3 in C3H10T1/2 cells promotes osteoblastic differentiation as indicated by the the induction of increase in alkaline phosphatase activity, an early marker of osteoblast differentiation, and increased expression of osteopontin, a late marker of osteogenesis. Glis3 acts synergistically with bone morphogenic protein 2 (BMP-2). In contrast, expression of Glis3 inhibits the induction of adipocyte differentiation. Microarray analysis identified the fibroblast growth factor 18 (FGF18) as one of the genes induced by Glis3 in C3H10T1/2 cells directly. Keywords: Glis3, osteoblast differentiation, adipocyte differentiation, FGF18, BMP2
2007-05-22 | GSE5379 | GEO
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