JUN induction in osteoprogenitors
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ABSTRACT:
PROVIDER: PRJNA605098 | ENA |
REPOSITORIES: ENA
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Project description:Different osteoprogenitors (SSC, BCSP, Thy+) were sorted after 2 days of JUN induction, followed by RNA extraction and microarray analysis
2020-02-07 | GSE144829 | GEO
Project description:Prenatal dexamethasone exposure (PDE) has long-term consequences in bone development. we investigated how PDE exerts persistent effect on bone metabolism in mouse offspring. Our results showed that PDE offspring exhibited reduced bone mass, fewer osteoblasts and diminished osteoprogenitors proliferation.And PDE increased MKP-1 expression, while decreasing H3 lysine 9 dimethylation (H3K9me2) at Mkp-1 gene locus. Mechanistically, dexamethasone suppressed osteoprogenitors proliferation by upregulating MKP-1 expression, notably through the inhibition of H3K9me2 modifications, which promoted demethylation and transcriptional activation of the Mkp-1 gene. Importantly, restoring histone methylation balance with PFI-90 treatment blocked the inhibitory effects of PDE on MAPK signaling in osteoprogenitors, and mitigated the detrimental impact of PDE on osteoprogenitor proliferation and bone development in the offspring. Therefore,we performed ChIP-seq for H3K9me2 to identify its role in related epigenetic changes.
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Project description:To investigate cellular population heterogeneity, and gene expression in osteoprogenitors and other cell types (endothelial, osteogenic, immune) we isolate the calvarial periosteum and sagittal sutures as stem cell compartments that contribute to osteogenesis. We compare cell populations and gene expression between different ages of mouse, and also between different diets (ad libitum vs intermittent fasting)
2024-12-06 | GSE226681 | GEO
Project description:To further dissect whether and how activated JUN reconfigures the chromatin landscape, we performed Chromatin Immunoprecipitation (ChIP)-seq analyses for H3K4me1 and H3K27ac. Based on the significant increase of H3K27ac levels at H3K4me1+ sites, we identified 3,017 JUN-activated enhancers in JUN WT cells. In contrast, JUN AA fails to significantly induce H3K27ac accumulation at these regions. Their enrichment levels at JUN-activated enhancers were significantly decreased after JNKi treatment. Besides, these enhancers are directly driven by JUN, especially phosphorylated JUN.
2022-12-09 | GSE196345 | GEO
Project description:Rejuvenating aged osteoprogenitors for bone repair
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Project description:We found that JUN expression is increased in many human fibrotic diseases and that systemic induction of Jun in mice resulted in development of fibrosis of multiple organs. To identify the changes in chromatin accessibility associated with JUN, we worked with primary human fibrotic lung fibroblasts that have normal or Knock-out levels of JUN expression and performed ATAC-seq analysis in both of them. Meanwhile we also modified primary human normal lung fibroblasts with or without JUN over-expression induction, then processed ATAC-seq and ChIP-seq analysis.
2020-04-27 | GSE114844 | GEO
Project description:Clinical evidence has established that concomitant traumatic brain injury accelerates bone healing, but the underlying mechanism is unclear. This study showed that after TBI, injured neurons, mainly those in the hippocampus, released osteogenic microRNA (miRNA)-enriched exosomes, which targeted osteoprogenitors in bone to stimulate bone formation. Importantly, increased fibronectin expression on exosomal surface contributed to targeting of osteoprogenitors in bone by TBI exosomes, thereby implying that modification of the exosome surface fibronectin could be used in bone-targeted drug delivery. Together, our findings have established a novel role of central regulation in bone formation and a clear link between injured neurons and osteogenitors, both in animals and clinical settings.
2021-07-13 | PXD022126 | Pride
Project description:The oncogene c-Jun plays a key role in development and cancer. Yet, its role in cell fate decision remains poorly understood at the molecular level. Here we report that c-Jun confers different fate decisions upon mouse embryonic stem cells (mESCs) in adhesion vs suspension. We developed a Tet-on system for temporal induction of c-Jun expression by Doxycycline treatment in mESCs. We show that mESCs carrying the inducible c-Jun TetOn remain pluripotent and grow slowly in suspension with induction of c-Jun, while undergoing differentiation with normal proliferative potentials in adherence upon c-Jun induction. Apparently, c-Jun pushes mESCs in suspension into cell cycle arrest at G1/S, through the induction of Cdkn1a/b and Cdkn2/a/b/c. Despite cell cycle arrest, they can re-enter cell cycle upon plating on adhesive surface and grow into typical mESC colonies albeit at lower efficiency. These results demonstrate that mESCs respond to c-Jun differently in suspension or adherence. Our results suggest that cells in suspension may be more resistant to differentiation than in adherence.
2019-02-19 | GSE114381 | GEO
Project description:We found that JUN and SHH expression is increased in many human fibrotic diseases and that systemic induction of Jun in mice resulted in development of fibrosis of multiple organs. To identify the changes in chromatin accessibility associated with JUN and SHH, we worked with primary SSCL dermal fibroblasts that have normal or Knock-out levels of JUN expression and vismodegib treatment then performed ATAC-seq analysis in all of them.
2020-09-08 | GSE151943 | GEO
Project description:Time course analysis of c-Jun expression at 24h resulted in upregulation of a number of well-known fibrogenesis-associated factors. We compared the global gene expression pattern of mouse whole bone marrow after c-Jun induction in vivo at 24h with no induction and applied to standard Affymetrix mouse arrays.
2016-07-26 | E-GEOD-84838 | biostudies-arrayexpress