Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12183683_1.fastq.gz | Fastqsanger.gz | |||
| SRR12183683_2.fastq.gz | Fastqsanger.gz | |||
| SRR12183684_1.fastq.gz | Fastqsanger.gz | |||
| SRR12183684_2.fastq.gz | Fastqsanger.gz | |||
| SRR12183685_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Human embryonic stem cells (hESCs) and induced pluripotent stem cells (hiPSCs) hold great promise for applications in drug discovery and regenerative medicine. While tremendous ongoing efforts are focused on establishing more optimal cellular microenvironments for hESCs/hiPSCs to facilitate their differentiation into the specific phenotypical functions of interests, it is still challenging to systematically determine the optimal environment and the circumstances supporting each environment, due to a lack of control over the microenvironmental factors in a three-dimensional (3D) space. In this study, we developed a 3D cellular microenvironment plate (3D-CEP), which consisted of a polydimethylsiloxane (PDMS) microfluidic device combined with a thermo-responsive poly(N-isopropylacrylamide)-β-poly(ethylene glycol) (PNIPAAm-β-PEG) hydrogel (HG), as a platform for hESC/hiPSC culture and analysis. The HG/3D-CEP system enables tuning of both chemical and physical environmental cues as well as in situ monitoring of cells. H9-derived hESCs cultured in the HG/3D-CEP system maintained pluripotent marker expression for octamer-binding transcription factor 4 (OCT4), (sex determining region Y)-box 2 (SOX2), NANOG, stage-specific embryonic antigen 4 (SSEA4), and TRA-1-60, but did not express the differentiation marker SSEA1 under self-renewing conditions. Small variations between different test environments and their influence on the development of biological networks could be further examined using global gene expression techniques. We envision that this HG/3D-CEP system will serve as a versatile platform for developing targeted functional cell lines derived from hESCs/hiPSCs and facilitate advances in more precise drug screening and regenerative medicine
2016-10-24 | GSE80324 | 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: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:CEP-37440 at low concentration (1,000 nM) decreased the proliferation of the human inflammatory breast cancer (IBC) cell line FC-IBC02, while not affecting the proliferation of normal breast epithelial cells. CEP-37440 decreased the cell proliferation of FC-IBC02 by blocking the auto-phosphorylation kinase activity of FAK (Tyr 397). This cell line did not expressed ALK. In vivo, CEP-37440 significantly decreased FC-IBC02 breast tumor xenografts growth with maximum of 40% tumor growth inhibition. None of the FC-IBC02 breast xenografts mice treated with CEP-37440 developed brain metastasis in contrast to the control group in which 20% of the mice developed brain metastasis. Expression array analyses in FC-IBC02 cells showed that CEP-37440 affects the expression of genes related to apoptosis specifically related to the interferon signaling pathway. Cell proliferation assays were performed in the presence of several concentrations of CEP-37440 using IBC and triple negative breast cancer (TNBC) non-IBC cell lines. We studied the expression of total FAK1, phospho-FAK1 (Tyr 397), total ALK and phospho-ALK (Tyr 1604) in these cells by ELISA. FC-IBC02 cells were treated with 1,000 nM CEP-37440 during 48 h, and expression arrays were performed in order to define pathways dysregulated by CEP-37440.
2015-12-14 | E-GEOD-73285 | biostudies-arrayexpress
Project description:CEP-37440 at low concentration (1,000 nM) decreased the proliferation of the human inflammatory breast cancer (IBC) cell line FC-IBC02, while not affecting the proliferation of normal breast epithelial cells. CEP-37440 decreased the cell proliferation of FC-IBC02 by blocking the auto-phosphorylation kinase activity of FAK (Tyr 397). This cell line did not expressed ALK. In vivo, CEP-37440 significantly decreased FC-IBC02 breast tumor xenografts growth with maximum of 40% tumor growth inhibition. None of the FC-IBC02 breast xenografts mice treated with CEP-37440 developed brain metastasis in contrast to the control group in which 20% of the mice developed brain metastasis. Expression array analyses in FC-IBC02 cells showed that CEP-37440 affects the expression of genes related to apoptosis specifically related to the interferon signaling pathway.
2015-12-14 | GSE73285 | GEO
Project description:Human induced pluripotent stem cells (hIPSCs) represent a unique opportunity for regenerative medicine since they offer the prospect of generating unlimited quantities of cells for autologous transplantation as a novel treatment for a broad range of disorders. However, the use of hIPSCs in the context of genetically inherited human disease will require correction of disease-causing mutations in a manner that is fully compatible with clinical applications. We analyzed hiPSC line and genetically modified derivatives using high-density SNP array to investigate genomic instability associated reprogramming and genetic modification.
2011-09-01 | GSE31035 | GEO
Project description:N-glycosylation is an important post-translational modification involved in protein folding, signal transduction, extracellular matrix (ECM) organization and immune response. Recent evidence shows that SARS-CoV-2 Spike protein is highly glycosylated and it may be potential target in viral pathology and drug/vaccine design. Therefore, the N-glycoproteomic profiling of coronavirus and its infected cells are of great importance in therapeutic targets screening for drug discovery. Here, we carried out 4D label-free LC-MS/MS-based N-glycoproteomics using a well-established SARS-CoV-2 cellular model, pangolin GX_P2V virus-infected Vero E6 cells, to study the mechanism of coronavirus infestation and potential drug targets. Meanwhile, we investigated the effect of Cepharanthine (CEP) on viral-induced aberrant N-glycoprotein changes in affected cells and on the viral proteins. The results showed that coronavirus GX_P2V could cause aberrant glycosylation of cell proteins at multiple levels, including extracellular matrix (ECM) and related signal transduction, whereas CEP can maintain 12 out of 69 GX_P2V-induced aberrant glycoproteins at normal glycosylation state. Functional enrichment and PPI analyses revealed that LAMB1 and FN1 were the pivotal proteins in regulating the aberrant glycosylation caused by coronavirus in presence of CEP, indicating that CEP might achieve its therapeutic intervention via these potential targets. Besides, CEP can regulate the glycosylation of viral proteins S, M and N. Nevertheless, there were still 57 out of 69 glycoproteins which cannot be significantly affected by CEP, indicating the combination of CEP with other drugs against the rest of targets should be considered.
2022-08-12 | PXD021297 | Pride
Project description:Acupuncture treatment is based on acupoint stimulation; however, the biological basis is not understood. We stimulated one acupoint with catgut embedding (CEP) for 8 weeks and then used isobaric tags for relative and absolute quantitation to screen proteins with altered expression in adjacent acupoints of Sprague Dawley rats. The expression levels of 10 proteins, including kininogen (KNG), consistently changed >1.5-fold in all three acupoints in CEP versus sham CEP-treated rats. Eight-week, but not 3-day, CEP treatment enhanced KNG expression. The enhanced KNG expression among small vessels in the subcutaneous layer was revealed via immunofluorescence. Nitric oxide synthesis was enhanced similar to KNG. These findings uncover biological changes at acupoints and suggest the critical role of the KNG–nitric oxide signaling pathway in acupoint activation.
2022-02-16 | PXD024018 | Pride
Project description:Cornelia de Lange syndrome (CdLS) is an autosomal dominant disease mainly caused by mutations in the Nipped-B-like protein (NIPBL) gene resulting in the alteration of the cohesin pathway. Here, we generated human induced pluripotent stem cells (hiPSCs) from a CdLS patient carrying a mutation in the NIPBL gene, c.5483G>A, and tested CRISPR-Cas based approaches to repair the genetic defect. We applied an efficient and precise method of gene correction through CRISPR-Cas induced homology directed repair (HDR), which allowed the generation of hiPSC clones with regular karyotype and preserved stemness. The efficient and precise gene replacement strategy developed in this study can be extended to the modification of other genomic loci in hiPSCs. Isogenic wild-type and mutated hiPSCs produced with the CRISPR-Cas technology are fundamental CdLS cellular models to study the disease molecular determinants and identifying therapeutic targets.
2023-03-17 | E-MTAB-11604 | 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