Expression and alternative splicing data of cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia
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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 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.
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.
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.
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.
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.
Project description:HIF-1A and HIF-2A regulate both overlapping and unique target genes in response to hypoxia. In this dataset, we identify specific HIF-1A and HIF-2A target genes in glioblastoma cells. 12 samples were analysed comprising 4 experimental conditions (normoxia scr, hypoxia scr, hypoxia siHIF1, hypoxia siHIF2) in triplicate. We made pairwise comparisons between the averages of each triplicate set to normoxia scr using the Partek suite.
Project description:This study explores the long-term adaptation mechanisms of lymphoma cells subjected to hypoxic conditions, with an emphasis on the HBL2 and Ramos cell lines under normoxia and 1% O2 environments. The research methodology encompassed lysing cells using a buffer containing sodium deoxycholate and TEAB, followed by protein quantification via a BCA assay. Subsequent steps involved protein digestion with trypsin, labelling with TMTpro™ 16plex Label Reagent Set for quantitative analysis, peptide fractionation, and LC-MS/MS analysis. The analytical process was supported by Proteome Discoverer 2.4 for protein identification and quantification. Experimental groups were categorized into "HBL2 normoxia," "HBL2 1% O2 adaptation," "Ramos normoxia," and "Ramos 1% O2 adaptation," conducted in triplicates to ensure reliability. This meticulous approach facilitated the delineation of unique proteomic landscapes indicative of hypoxia adaptation, unveiling cellular strategies employed by lymphoma cells to navigate low oxygen conditions. The findings advance our comprehension of how hypoxia influences cancer progression and potentially opens new avenues for targeting hypoxic niches within tumors.
Project description:Lysates of Mycobacterium tuberculosis (H37Rv auxotroph mc(2)6020) grown under various conditions (normoxia, hypoxia, reactivation from hypoxia) probed the serine hydrolase probe with ActivX-desthiobiotin FP.
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.
Project description:We studied how Fusobacterium nucleatum infection under hypoxia regulated the epigenome and transcriptome of colon cancer cells. The six datasets that are described in this study are labeled as follows: (a) Normoxia - No Bacteria (NN), (b) Normoxia - infection with Fnn (NF), (c) Normoxia - infection with E. coli (NE), (d) Hypoxia - No Bacteria (HN), (e) Hypoxia - infection with Fnn (HF), and (f) Hypoxia - infection with E. coli (HE).
Project description:We studied how Fusobacterium nucleatum infection under hypoxia regulated the epigenome and transcriptome of colon cancer cells. The six datasets that are described in this study are labeled as follows: (a) Normoxia - No Bacteria (NN), (b) Normoxia - infection with Fnn (NF), (c) Normoxia - infection with E. coli (NE), (d) Hypoxia - No Bacteria (HN), (e) Hypoxia - infection with Fnn (HF), and (f) Hypoxia - infection with E. coli (HE).