Expression data of osteogenic differentiated cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE83284 | GEO | 2016/06/14
SECONDARY ACCESSION(S): PRJNA325486
REPOSITORIES: GEO
Similar Datasets
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. Human cartilage endplate-derived stem cells (CESCs) were treated with osteogenic differentiation medium under normoxia and hypoxia for 21 days respectively.
2016-06-14 | E-GEOD-83284 | biostudies-arrayexpress
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
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.
2016-07-18 | GSE84484 | GEO
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
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.
2015-12-21 | GSE63897 | GEO
Project description:The degeneration of cartilage endplate in cervical disc is considered as a basis of cervical spondylosis. Owing to the important role of post-transcriptional gene regulation in phenotypes and functions of cells, non-coding ribonucleic acid (ncRNA) molecules contributed to the regulation.Degenerated cervical vertebral endplate cartilage specimens were collected from patients with cervical intervertebral disc degeneration (CIDD) that suffered from cervical spondylosis myelopathy, who had received anterior cervical discectomy and fusion (ACDF). CE specimens of healthy subjects were obtained from patients with a cervical fracture who received ACDF at The Second Affiliated Hospital of Nanchang University (Nanchang, China) and adopted SBC human ceRNA array V1.0（4×180K）. The results revealed that expressions of369 lncRNAs, 246 mRNAs, 578 circRNAs were different between degenerated cartilage endplate and healthy cartilage endplate. The functions of differentially expressed lncRNAs and co-expressed potential targeting genes were predicted by analyzing Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) biological pathway analysis. Furthermore, we analyzed and find the co-expression and interaction patterns of different RNAs and possible ceRNA mechanism. The present study provided a systematic perspective on the potential function of non-coding RNAs (ncRNAs) in the degeneration of cartilage endplate in CIDD.
2020-07-04 | GSE153761 | GEO
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
Project description:Background: Low back pain is a leading cause of disability worldwide and is frequently attributed to intervertebral disc (IVD) degeneration. Though the contributions of the adjacent cartilage endplates (CEP) to IVD degeneration are well documented, the phenotype and functions of the resident CEP cells are critically understudied. To better characterize CEP cell phenotype and possible mechanisms of CEP degeneration, bulk and single-cell RNA-Sequencing of non-degenerated and degenerated CEP cells were performed. Methods: Human lumbar CEP cells from degenerated (Thompson Grade ≥ 4) and non-degenerated (Thompson Grade ≤ 2) discs were expanded for bulk (N=4 non-degenerated, N=4 degenerated) and single-cell (N=1 non-degenerated, N=1 degenerated) RNA-Sequencing. Genes identified from bulk RNA-Sequencing were categorized by function and their expression in non-degenerated and degenerated CEP cells were compared. A PubMed literature review was also performed to determine which genes were previously identified and studied in the CEP, IVD, and other cartilaginous tissues. For single-cell RNA-Sequencing, different cell clusters were resolved using unsupervised clustering and functional annotation. Differential gene expression analysis and Gene Ontology, respectively, were used to compare gene expression and functional enrichment between cell clusters, as well as between non-degenerated and degenerated CEP samples. Results: Bulk RNA-Sequencing revealed 38 genes were significantly upregulated and 15 genes were significantly downregulated in degenerated CEP cells relative to non-degenerated cells (|Fold change| ≥ 1.5). Of these, only 2 genes were previously studied in CEP cells and 31 were previously studied in the IVD and other cartilaginous tissues. Single-cell RNA-Sequencing revealed 11 unique cell clusters, including multiple chondrocyte and progenitor subpopulations with distinct gene expression and functional profiles. Analysis of genes in the bulk RNA-Sequencing dataset showed that progenitor cell clusters from both samples were enriched in “non-degenerated” genes, but not “degenerated” genes. For both bulk- and single-cell analyses, gene expression and pathway enrichment analyses highlighted several pathways that may regulate CEP degeneration, including transcriptional regulation, translational regulation, intracellular transport, and mitochondrial dysfunction. Conclusions: This thorough analysis using RNA-Sequencing methods highlighted numerous differences between non-degenerated and degenerated CEP cells, the phenotypic heterogeneity of CEP cells, and several pathways of interest that may be relevant in CEP degeneration.
2024-01-10 | GSE242040 | GEO
Project description:Background: Low back pain is a leading cause of disability worldwide and is frequently attributed to intervertebral disc (IVD) degeneration. Though the contributions of the adjacent cartilage endplates (CEP) to IVD degeneration are well documented, the phenotype and functions of the resident CEP cells are critically understudied. To better characterize CEP cell phenotype and possible mechanisms of CEP degeneration, bulk and single-cell RNA-Sequencing of non-degenerated and degenerated CEP cells were performed. Methods: Human lumbar CEP cells from degenerated (Thompson Grade ≥ 4) and non-degenerated (Thompson Grade ≤ 2) discs were expanded for bulk (N=4 non-degenerated, N=4 degenerated) and single-cell (N=1 non-degenerated, N=1 degenerated) RNA-Sequencing. Genes identified from bulk RNA-Sequencing were categorized by function and their expression in non-degenerated and degenerated CEP cells were compared. A PubMed literature review was also performed to determine which genes were previously identified and studied in the CEP, IVD, and other cartilaginous tissues. For single-cell RNA-Sequencing, different cell clusters were resolved using unsupervised clustering and functional annotation. Differential gene expression analysis and Gene Ontology, respectively, were used to compare gene expression and functional enrichment between cell clusters, as well as between non-degenerated and degenerated CEP samples. Results: Bulk RNA-Sequencing revealed 38 genes were significantly upregulated and 15 genes were significantly downregulated in degenerated CEP cells relative to non-degenerated cells (|Fold change| ≥ 1.5). Of these, only 2 genes were previously studied in CEP cells and 31 were previously studied in the IVD and other cartilaginous tissues. Single-cell RNA-Sequencing revealed 11 unique cell clusters, including multiple chondrocyte and progenitor subpopulations with distinct gene expression and functional profiles. Analysis of genes in the bulk RNA-Sequencing dataset showed that progenitor cell clusters from both samples were enriched in “non-degenerated” genes, but not “degenerated” genes. For both bulk- and single-cell analyses, gene expression and pathway enrichment analyses highlighted several pathways that may regulate CEP degeneration, including transcriptional regulation, translational regulation, intracellular transport, and mitochondrial dysfunction. Conclusions: This thorough analysis using RNA-Sequencing methods highlighted numerous differences between non-degenerated and degenerated CEP cells, the phenotypic heterogeneity of CEP cells, and several pathways of interest that may be relevant in CEP degeneration.
2024-01-10 | GSE242443 | GEO
Project description:Expression data of osteogenic differentiated cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia
| PRJNA325486 | ENA