E-MTAB-8536
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ABSTRACT:
PROVIDER: E-MTAB-8536 | ExpressionAtlas | 2020-01-13
REPOSITORIES: ExpressionAtlas
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Project description:RNA-seq of murine mesenchymal stem cells during differentiation to osteoblasts, treated with tofacitinib or baricitinib against vehicle control
| PRJEB35487 | ENA
Project description:Schittler2010 - Cell fate of progenitor cells, osteoblasts or chondrocytes
Mathematical model describing the mechanism of differentiation of mesenchymal stem cells to bone (osteoblasts) or cartilage (chondrocytes) cells.
This model is described in the article:
Cell differentiation modeled via a coupled two-switch regulatory network.
Schittler D, Hasenauer J, Allgöwer F, Waldherr S.
Chaos 2010 Dec; 20(4): 045121
Abstract:
Mesenchymal stem cells can give rise to bone and other tissue cells, but their differentiation still escapes full control. In this paper we address this issue by mathematical modeling. We present a model for a genetic switch determining the cell fate of progenitor cells which can differentiate into osteoblasts (bone cells) or chondrocytes (cartilage cells). The model consists of two switch mechanisms and reproduces the experimentally observed three stable equilibrium states: a progenitor, an osteogenic, and a chondrogenic state. Conventionally, the loss of an intermediate (progenitor) state and the entailed attraction to one of two opposite (differentiated) states is modeled as a result of changing parameters. In our model in contrast, we achieve this by distributing the differentiation process to two functional switch parts acting in concert: one triggering differentiation and the other determining cell fate. Via stability and bifurcation analysis, we investigate the effects of biochemical stimuli associated with different system inputs. We employ our model to generate differentiation scenarios on the single cell as well as on the cell population level. The single cell scenarios allow to reconstruct the switching upon extrinsic signals, whereas the cell population scenarios provide a framework to identify the impact of intrinsic properties and the limiting factors for successful differentiation.
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2013-11-19 | BIOMD0000000493 | BioModels
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Project description:Rosiglitazone-targeted transcriptional networks as gene expression signature of physiological and pathological mineralization – a top-down approach to identify novel targets for bone and vascular health Clinical studies have recently revealed detrimental skeletal and vascular effects of the insulin sensitizer rosiglitazone. At the cellular level, we have shown earlier that rosiglitazone accelerates osteoblast differentiation from human mesenchymal stem cells (hMSC) at the expense of increased oxidative stress and apoptosis. In calcifying human vascular cells, rosiglitazone stimulates pathological mineralization, an effect that was diminished by the antioxidant resveratrol. In order to elucidate the transcriptional networks underlying the rosiglitazone-enhanced mineralization phenotype, we performed genome-wide transcriptional profiling of osteogenic hMSCs treated with rosiglitazone for short-term periods of 1 up to 48h during the first two days of culture time, a phase that we show is sufficient to mediate the stimulatory effect of rosiglitazone on mineralization. Microarray-based mRNA expression analysis revealed 190 probes that were differently expressed in at least one condition compared to vehicle-treated control. This rosiglitazone gene signature contained confirmed primary PPAR targets and was also endogenously regulated during osteogenic differentiation from hMSCs and osteoblast-like differentiation of vascular smooth muscle cells (VSMCs) into calcifying vascular cells (CVCs). Further comparative analysis revealed rosiglitazone targets that were commonly enriched in osteoblasts and CVCs or specifically enriched in either osteoblasts or CVCs. Finally, we compared the expression patterns of CVC-specific genes with patient expression data from carotid plaque versus intact adjacent tissue, and identified five rosiglitazone targets that were differentially regulated in CVCs and carotid plaque but not osteoblasts when compared to their respective non-mineralizing counterparts. These targets, i.e PDK4, SDC4, SPRY4, TCF4, and DACT1 may specifically control extracellular matrix mineralization in vascular cells and hence provide interesting candidates for further investigations to improve vascular health.
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Project description:The effect of parathyroid hormone (PTH) treatment was tested on osteoblasts prepared from calvaria of C57BL/6J mice 7-10 days old. Osteoblasts were treated with either human parathyroid hormone (1-34), bovine (D-Trp12,Tyr34) parathyroid hormone (7-34) amide or vehicle control for 4 hr. Gene expression effects were evaluated by DNA microarray.
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