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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data of osteogenic differentiated cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia

ABSTRACT: Cartilage endplate-derived stem cells (CESCs) with chondro-osteogenic differentiation capacity may be responsible for the balance of chondrification and ossification in cartilage endplate (CEP). CEP is an avascular and hypoxic tissue, and hypoxia could inhibit the osteogenic differentiation of CESCs. We used high-throughput scanning to identify differentially expressed genes (DEGs) and alternatively spliced genes (ASGs) during osteogenic differentiation of CESCs under hypoxia compared to those induced under normoxia. Human cartilage endplate-derived stem cells (CESCs) were treated with osteogenic differentiation medium under normoxia and hypoxia for 21 days respectively.

ORGANISM(S): Homo sapiens

SUBMITTER: Yuan Yao

PROVIDER: E-GEOD-83284 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression and alternative splicing data of cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia

Project description:Cartilage endplate-derived stem cells (CESCs) with chondro-osteogenic differentiation capacity may be responsible for the balance of chondrification and ossification in cartilage endplate (CEP). CEP is an avascular and hypoxic tissue, and hypoxia could influence the fate of CESCs. We used high-throughput scanning to identify differentially expressed genes (DEGs) and alternatively spliced genes (ASGs) of CESCs under hypoxia compared to those under normoxia. Human cartilage endplate-derived stem cells (CESCs) were cultured under normoxia and hypoxia for 21 days respectively.

2016-07-18 | E-GEOD-84484 | biostudies-arrayexpress

Expression data of osteogenic differentiated cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia

Project description:Cartilage endplate-derived stem cells (CESCs) with chondro-osteogenic differentiation capacity may be responsible for the balance of chondrification and ossification in cartilage endplate (CEP). CEP is an avascular and hypoxic tissue, and hypoxia could inhibit the osteogenic differentiation of CESCs. We used high-throughput scanning to identify differentially expressed genes (DEGs) and alternatively spliced genes (ASGs) during osteogenic differentiation of CESCs under hypoxia compared to those induced under normoxia.

2016-06-14 | GSE83284 | GEO

Expression and alternative splicing data of cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia

2016-07-18 | GSE84484 | GEO

Gene expression and alternative splicing data from human cartilage endplate-derived stem cells

Project description:Low back pain (LBP) is one of the most prevalent conditions which need medical advice and result in chronic disabilities. Degenerative disc disease (DDD) is a common reason for LBP. A lot of researchers think that CEP degeneration play critical roles in the initiation and development of DDD. In recent years, researchers have put interests on cell-based therapies for regenerating disc structure and function. Our research team has isolated cartilage endplate-derived stem cells (CESCs) and validated their chondrogenic and osteogenic differentiation ability. Enhanced chondrogenic differentiation and inhibited osteogenic differentiation of CESCs may retard CEP calcification and restore the nutrition supply, possibly regenerating the degenerated discs. We used Affymetrix Human Transcriptome Array 2.0 to study the global gene expression profilling and alternative splicing events during the chondrogenic and osteogenic differentiation of cartilage endplate-derived stem cells. The cartilage endplate-derived stem cells(CESCs) were induced to undergo chondrogenic(CD) and osteogenic differentiation(OD). Both undifferentiated and differentiated CESCs were sent for RNA extraction and hybridization on Affymetrix microarrays. A comparative analysis was done between the undifferentiated and differentiated samples.

2015-12-21 | E-GEOD-63897 | biostudies-arrayexpress

Gene expression and alternative splicing data from human cartilage endplate-derived stem cells

2015-12-21 | GSE63897 | GEO

Homo sapiens

Project description:Expression data of osteogenic differentiated cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia

| PRJNA325486 | ENA

Transcriptomic changes in C3H10T1/2 cells exposed to lipid deprivation

Project description:The avascular nature of cartilage makes it a unique tissue in the human body, but whether and how the absence of blood vessels regulates chondrogenesis remains unknown. Obstruction of vascular invasion during bone healing favours chondrogenic over osteogenic differentiation of skeletal progenitor cells, a process we observed to be driven by a decreased availability of extracellular lipids. To understand how lipid deprivation activates the chondrogenic programme, we profiled mRNA expression of C3H10T1/2 skeletal progenitors exposed to lipid deprivation for 1, 3 or 6 hours.

2019-12-09 | E-MTAB-7564 | biostudies-arrayexpress

Analysis of gene expression changes in response to hypoxia and/or cisplatin in A2780 and A2780cis cells

Project description:The aim of this experiment was to evaluate the changes in gene expression in response to hypoxia and/or cisplatin in an ovarian cancer cell line model. A2780 (cisplatin-sensitive) and A2780cis (cisplatin-resistant) cell lines were treated with cisplatin in normoxia or hypoxia (0.5% O2) for 72 hours. RNA was extracted from three independent biological replicates for each condition: A2780 (normoxia, untreated); A2780 (hypoxia, untreated); A2780 (normoxia, cisplatin); A2780cis (hypoxia, cisplatin), A2780cis (normoxia, untreated); A2780cis (hypoxia, untreated); A2780cis (normoxia, cisplatin); A2780cis (hypoxia, cisplatin) and interrogated on Affymetrix Human Gene ST 1.0 arrays.

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Hypoxia promotes osteogenesis via regulating the acetyl-CoA-mediated mito-nuclear communication.

Project description:Bone-mesenchymal stem cells (MSCs) reside in a hypoxic niche that maintains their differentiation potential. Although the role of hypoxia (low oxygen concentration) in the regulation of stem cell function has been previously reported, with normoxia (high oxygen concentration) leading to impaired osteogenesis, the molecular events triggering changes in stem cell fate decisions in response to high oxygen remain elusive. Here, we study the impact of normoxia on 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 metabolic rewiring resulting in high acetyl-CoA levels, histone hypo-acetylation occurs due to trapping of acetyl-CoA inside mitochondria, owing to lower CiC activity. Strikingly, restoring the cytosolic acetyl-CoA pool 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 the MSC function.

2022-08-01 | ST002242 | MetabolomicsWorkbench

Transcriptomic profiling of wild-type and Bmal1-/- myoblasts under normoxia or actue hypoxia conditions

Project description:Purpose: The goal of this study is to investigate the role of interplay between circadian clock and oxygen-sensing pathways in determining myogenic progenitor cell fate. Methods: Total RNAs were extracted from wild-type and Bmal1-/- myoblasts following exposure to normoxia (21% O2) or hypoxia (1% O2) for 6 hours, and subjected to RNA-sequencing. Results: There were significantly up-regulated (443 in normoxia versus 477 in hypoxia) and down-regulated (745 in normoxia versus 796 in hypoxia) genes in Bmal1-/- cells compared to wild-type, with a large degree of overlap between hypoxia and normoxia, although the fold change of differential gene expression was generally greater under hypoxia versus normoxia. Conclusion: Loss of Bmal1 in myoblasts leads to a premature differentiation-prone transcriptome, which was exaggerated following exposure to hypoxia.

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