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Deregulated mito-nuclear communication alters chromatin plasticity and osteogenic differentiation potential upon ageing in mesenchymal stem cells (MSCs) [RNA-seq]

ABSTRACT: Deregulated mito-nuclear communication alters chromatin plasticity and osteogenic differentiation potential upon ageing in mesenchymal stem cells (MSCs) [RNA-seq]

PROVIDER: PRJNA600978 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10880603.fastq.gz	Fastqsanger.gz
	SRR10880604.fastq.gz	Fastqsanger.gz
	SRR10880605.fastq.gz	Fastqsanger.gz
	SRR10880606.fastq.gz	Fastqsanger.gz
	SRR10880607.fastq.gz	Fastqsanger.gz

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Deregulated mito-nuclear communication alters chromatin plasticity and osteogenic differentiation potential upon ageing in mesenchymal stem cells (MSCs)

Project description:Deregulated mito-nuclear communication alters chromatin plasticity and osteogenic differentiation potential upon ageing in mesenchymal stem cells (MSCs)

| PRJNA600973 | ENA

Deregulated mito-nuclear communication alters chromatin plasticity and osteogenic differentiation potential upon ageing in mesenchymal stem cells (MSCs) [ATAC-seq]

Project description:Deregulated mito-nuclear communication alters chromatin plasticity and osteogenic differentiation potential upon ageing in mesenchymal stem cells (MSCs) [ATAC-seq]

| PRJNA600975 | ENA

Deregulated mito-nuclear communication alters chromatin plasticity and osteogenic differentiation potential upon ageing in mesenchymal stem cells (MSCs)

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-08 | GSE143580 | GEO

Deregulated mito-nuclear communication alters chromatin plasticity and osteogenic differentiation potential upon ageing in mesenchymal stem cells (MSCs) [RNA-seq]

Project description:We report that upon ageing MSC undergo a metabolic switc, down-regulating glycolysis and inducing fatty acid oxidation, which results in elevated acetyl-CoA levels. However, aged cells exhibit chromatin compaction and histone hypo-aceylation. This is due to the lower levels of citrate carrier, resulting in impaired acetyl-CoA export from mitochondria to the cytosol, which concomitantly affetcs histone acetylation and osteogenesis.

2021-07-08 | GSE143579 | GEO

Deregulated mito-nuclear communication alters chromatin plasticity and osteogenic differentiation potential upon ageing in mesenchymal stem cells (MSCs) [ATAC-seq]

2021-07-08 | GSE143578 | GEO

Hypoxia promotes osteonesis via regulation of the mito-nuclear communication [ChIP-seq]

Project description:Bone marrow mesenchymal stem cells (MSCs) reside in a hypoxic niche that maintains their differentiation potential. Several studies have highlighted the critical role of hypoxia (low oxygen concentration) in the regulation of stem cell function, reporting differentiation defects following a switch to normoxia (high oxygen concentration). However, the molecular events triggering changes in stem cell fate decisions in response to high oxygen remain elusive. Here, we study the impact of normoxia in the mito-nuclear communication, with regards to stem cell differentiation. We show that normoxia-cultured MSCs undergo profound transcriptional alterations which cause irreversible osteogenesis defects. Mechanistically, high oxygen promotes chromatin compaction and histone hypo-acetylation, particularly on promoters and enhancers of osteogenic genes. Although normoxia induces rewiring of metabolism, resulting in high acetyl-CoA levels, histone hypo-acetylation occurs due to trapping of acetyl-CoA inside mitochondria, likely due to lower CiC activity. Strikingly, restoring the cytosolic acetyl-CoA pool via acetate supplementation remodels the chromatin landscape and rescues the osteogenic defects. Collectively, our results demonstrate that the metabolism-chromatin-osteogenesis axis is heavily perturbed in response to high oxygen and identify CiC as a novel, oxygen-sensitive regulator of MSC function.

2022-10-18 | GSE200071 | GEO

Hypoxia promotes osteonesis via regulation of the mito-nuclear communication [RNA-seq]

2022-10-18 | GSE200070 | GEO

Hypoxia promotes osteonesis via regulation of the mito-nuclear communication [ATAC-seq]

2022-10-18 | GSE200072 | GEO

Expression profiling of microRNAs during osteogenic differentiation of human MSCs

Project description:The goal of this study was to determine expression profiles of microRNAs (miRNAs) in whole cell extracts of human bone marrow-derived mesenchymal stem/stromal cells (MSCs) as well as in MSCs during osteogenic differentiation. MicroRNAs are epigenetic regulators that commonly function by targeting specific mRNAs resulting in suppression of protein expression and modulation of a number of cellular pathways. This experiment is part of a larger study analyzing the expression of mitochondria-associated miRNAs in MSCs during osteogenesis that we recently submitted to GEO (Series GSE134946). Here, the same three human MSC lines were used in this study, under the same osteogenic induction conditions, to generate expression profiles of miRNAs present in whole cell extracts. A standard in vitro osteogenesis assay system was used to differentiate MSCs toward the osteoblast lineage.Purified whole cell extracts were obtained from MSCs or from MSCs at specific time points of osteogenic induction. RNA was isolated from whole cell extracts and then biotin-labeled in preparation for microRNA array (Affymetrix miRNA array 4.0). Array data was analyzed to generate information on most abundantly-expressed miRNAs in non-induced MSCs as well as in MSCs at set time points (day 3, 7, or 14) of osteogenic induction. Information on significantly differentially-expressed miRNAs during osteogenesis (comparing day 0 with either day 3, 7 or 14) was also obtained.

2021-01-01 | GSE148049 | GEO

Expression profiling of mitochondria-associated microRNAs during osteogenic differentiation of human MSCs

Project description:The goal of this study was to determine expression profiles of mitochondria-associated microRNAs (mitomiR) in human bone marrow-derived mesenchymal stem/stromal cells (MSCs) as well as in MSCs during osteogenic differentiation. MicroRNAs are epigenetic regulators that commonly function by targeting specific mRNAs resulting in suppression of protein expression. In addition to their location in the cytosol, microRNAs have also been found in other sub-cellular compartments including the mitochondria. While some studies suggest that mitomiRs may affect mitochondrial function, research on mitomiRs is still in its infancy. To date, there is no information on mitomiR expression in MSCs or osteoblasts. A standard in vitro osteogenesis assay system was used to differentiate MSCs toward the osteoblast lineage. Purified mitochondrial extracts were obtained from MSCs or from MSCs at specific time points of osteogenic induction. RNA was isolated from mitochondrial extracts and then biotin-labeled in preparation for microRNA array (Affymetrix miRNA array 4.0). Array data was analyzed to generate information on most abundantly-expressed mitomiRs in non-induced MSCs as well as in MSCs at set time points (day 3, 7, or 14) of osteogenic induction. Information on significantly differentially-expressed mitomiRs during osteogenesis (comparing day 0 with either day 3, 7 or 14) was also obtained.

2020-01-01 | GSE134946 | GEO

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