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Gene expression alteration in chondrocyte by A-CEBP overexpression.

ABSTRACT: To investigate loss-of-function of the C/EBP family members, we used A-CEBP which exerts a dominant-negative effect against all CEBPs. DOX-inducible overexpression of A-CEBP into mouse chondrocyte cell line ATDC5 increased expressions of early differentiation markers, decreased those of late differentiation markers. In addition, A-CEBP altered many genes related with skeletal development, cartilage, cell cycle, inflammation and apoptosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE60651 | GEO | 2014/11/01

SECONDARY ACCESSION(S): PRJNA259197

REPOSITORIES: GEO

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Gene expression alteration in chondrocyte by A-CEBP overexpression.

Project description:To investigate loss-of-function of the C/EBP family members, we used A-CEBP which exerts a dominant-negative effect against all CEBPs. DOX-inducible overexpression of A-CEBP into mouse chondrocyte cell line ATDC5 increased expressions of early differentiation markers, decreased those of late differentiation markers. In addition, A-CEBP altered many genes related with skeletal development, cartilage, cell cycle, inflammation and apoptosis. We established stable ATDC5 cells which express GFP or A-CEBP by DOX induction. We started differentiation of these cells by ITS supplement immediately after DOX induction, harvested mRNA after 3 weeks, and performed microarray analysis.

2014-11-01 | E-GEOD-60651 | biostudies-arrayexpress

Gene expression alteration in chondrocyte by HES1 overexpression

Project description:To investigate target molecules of HES1, we transduced GFP or HES1 into mouse chondrocyte cell line ATDC5, and performed the microarray analysis. HES1 overexpression increased inflammation-related genes including Il6 and Il1rl1. We established stable ATDC5 cells overexpressing GFP or HES1 by lentiviral transduction. We harvested mRNA from these cells, and performed microarray analysis.

2015-03-02 | E-GEOD-60737 | biostudies-arrayexpress

Gene expression alteration in chondrocyte by HES1 overexpression

2015-03-02 | GSE60737 | GEO

Transcription profiling by array of human myometrial cells transfected by NFKB (p65) and CEBP alone and in combination.

Project description:Nuclear factor kappa B and C/EBP are two important transcription factors that independently and synergistically regulate different genes. In this experiment the expression of genes will be examined with the overexpression of NFKB (p65) and CEBP alone and in combination.

2010-03-24 | E-MEXP-2160 | biostudies-arrayexpress

Genome-wide transcriptome profiling of wild-type and Kmt2d-deficient ATDC5 differentiated chondrocytes and undifferentiated mesenchymal cells

Project description:We performed genome-wide transcriptome profiling in stable Kmt2d-/- (bi-allelic deletion of the catalytic SET domain) and Kmt2d+/+ ATDC5 chondrocyte cell lines 7 days after induction of differentiation and in stable Kmt2d-/- and Kmt2d+/+ undifferentiated ATDC5 cells.

2019-10-09 | GSE129365 | GEO

Expression Data from ATDC5 cells treated with Yoda1

Project description:Chondrocytes can potentially perceive mechanical stimuli via Piezo channels. We investigated the effect of the Piezo1 agonist Yoda1 on chondrocyte-like ATDC5 cells. Chondrocytes can potentially perceive mechanical stimuli via Piezo channels. We investigated the effect of the Piezo1 agonist Yoda1 on chondrocyte-like ATDC5 cells. Chondrocytes can potentially perceive mechanical stimuli via Piezo channels. We investigated the effect of the Piezo1 agonist Yoda1 on chondrocyte-like ATDC5 cells. Chondrocytes can potentially perceive mechanical stimuli via Piezo channels. We investigated the effect of the Piezo1 agonist Yoda1 on chondrocyte-like ATDC5 cells. We used microarray analysis to detail the global gene expression of ATDC5 cells in response to 6 hours of treatment with 5µM Yoda1.

2024-02-28 | GSE230071 | GEO

ChIP-seq analysis of the C. elegans CEBP-1 protein

Project description:Purpose: The goal of this study is to identify genes selectively associated with C. elegans CEBP-1. Methods: We generated transgenic animals expressing FLAG-tagged CEBP-1 in a cebp-1(tm2807) mutant background (cebp-1(0); juIs418 [Pcebp-1::FLAG::CEBP-1::cebp-1 3’UTR]) and then immunoprecipitated FLAG-CEBP-1-associated DNA fragments using anti-FLAG antibodies (M2 anti-FLAG magnetic beads; Sigma). We collected mixed stage worms grown at 20˚C on NGM plates followed by 2% formaldehyde and sonicated the samples as described (Mukhopadhyay et al., 2008). We next generated ChIP-seq DNA libraries. Briefly, both ChIPed DNA and input genomic DNA were ligated to specific adaptors and amplified by barcode primers followed by sequencing on the Illumina HiSeq-2000 platform. We performed two independent ChIP-seq experiments, with parallel genomic DNA controls prepared from the same strain. We conducted peak-calling using CLC genomics workbench 6.0 (CLCbio). To define genes associated with the peaks, we used the annotation of transcription start site (TSS) and transcription end site (TES) from WS220 and annotated the peak if it overlapped the gene or the 3 kb upstream of the TSS. We then manually confirmed the peaks and associated genes using UCSC browser and update to WS252. Results: We found 209 CEBP-1 ChIP-seq peaks in the genome that were associated with 212 coding genes. Through motif discovery tools, we also found that CEBP-1 binds conserved DNA motifs. Conclusions: The conservation of C.elegans CEBP-1 binding motif supports functional parallels between C. elegans CEBP-1 and vertebrate C/EBPs.

2016-09-13 | GSE83330 | GEO

Gene expression alteration in murine chondrogenic cell line ATDC5 cells by IL-1β and Fascin1 inhibitor NP-G2-044 treatment

Project description:To investigate the protective effect of Fascin1 inhibitor NP-G2-044 against chondrocyte dedifferentiation, we stimulated murine chondrogenic cell line ATDC5 cells with IL-1β to induce dedifferentiation, and with or without NP-G2-044 treatment. Gene expression profiling analysis was performed using data obtained from RNA-seq of three independent experiments.

2023-05-27 | GSE232611 | GEO

An evolutionary recent IFN-IL-6-CEBP axis is linked to monocyte expansion and tuberculosis severity in humans.

Project description:Monocyte counts are increased during human tuberculosis (TB) but it has not been determined whether Mycobacterium tuberculosis (Mtb) directly regulates myeloid commitment. We demonstrated that exposure to Mtb directs primary human CD34+ cells to differentiate into monocytes/macrophages. In vitro myeloid conversion did not require type I or type II IFN signaling. In contrast, Mtb enhanced IL-6 responses by CD34+ cell cultures and IL-6R neutralization inhibited myeloid differentiation and decreased mycobacterial growth in vitro. Integrated systems biology analysis of transcriptomic, proteomic and genomic data of large data sets of healthy controls and TB patients established the existence of a myeloid IL-6/IL6R/CEBP gene module associated with disease severity. Furthermore, genetic and functional analysis revealed the IL6/IL6R/CEBP gene module has undergone recent evolutionary selection, including Neanderthal introgression and human pathogen adaptation, connected to systemic monocyte counts. These results suggest Mtb co-opts an evolutionary recent IFN-IL6-CEBP feed-forward loop, increasing myeloid differentiation linked to severe TB in humans.

2019-10-24 | GSE129270 | GEO

Uhrf1 is indispensable for normal limb growth by regulating chondrocyte differentiation

Project description:Chondrocyte differentiation is regulated at a transcriptional level and by various hormonal stimuli. Since chondrocyte differentiation is important for normal skeletal growth, inadequate amounts of differentiation can lead to pathological conditions such as osteoarthritis. Transcriptional regulation can be tightly orchestrated by epigenetic regulators. Among these, ubiquitin-like with PHD and RING finger domains 1 (Uhrf1) is reported to have diverse epigenetic functions, including regulation of DNA methylation. However, the physiological functions of Uhrf1 in skeletal tissues remain unclear. Here we show that limb mesenchymal cell-specific Uhrf1 conditional knockout mice (Uhrf1ΔLimb/ΔLimb) exhibit shortened long bones that have morphological deformities due to impaired chondrocyte differentiation and proliferation. RNA-seq performed on primary cultured chondrocytes obtained from control and Uhrf1ΔLimb/ΔLimb mice revealed that expression levels of proliferative chondrocyte marker genes were downregulated, whereas hypertrophic chondrocyte marker genes were upregulated. In addition, gene ontology analyses and Gene Set Enrichment Analysis (GSEA) suggested that limb growth retardation due to compromised chondrocyte differentiation might be caused by increased activity of the focal adhesion signaling pathway. These results indicated that Uhrf1 has a crucial role in normal skeletal maturation by coordinating transcriptional regulatory networks during chondrocyte differentiation.

2017-12-23 | GSE92641 | GEO

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