Gene expression profiling of the 414C2 iPSC line during hypertrophic chondrocyte induction
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ABSTRACT:
PROVIDER: PRJNA663541 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In order to better understand the mechanisms of chondrocyte hypertrophy, we induced hypertrophic chondrocytes from 414C2 iPSCs and analyzed their gene expression profile. This dataset includes the expression data obtained from iPSC-derived sclerotome and cartilage on days -1, 28, and 56 of induction. Day 56 samples were compared to day 28 samples to analyze pathways involved in chondrocyte hypertrophy.
2021-02-24 | GSE157955 | GEO
Project description:To investigate the role of collagen X in human chondrocytes, we established human induced pluripotent stem cells (hiPSC) with heterozygous (COL10A1+/-) or homozygous (COL10A1-/-) deletions of COL10A1 gene using dual guide RNAs and CRISPR/Cas9 system. Several mutant clones were established from each of two standard hiPSCs and differentiated into hypertrophic chondrocytes by the previously reported 3D induction method. Transcriptome analyses of chondrocyte pellets at the hypertrophic phase showed lower expression of proliferating-phase genes and higher expression of calcification-phase genes in COL10A1-/- pellets than in parental cell pellets.
2023-12-01 | GSE218830 | GEO
Project description:In order to better understand chondrodysplasia disease mechanisms, we induced hypertrophic chondrocytes from chondrodysplasia-specific iPSCs and analyzed their gene expression profile. This dataset includes the expression data obtained from iPSC-derived cartilage pellets on day 56 of hypertrophic induction. Three COL10A1 mutants and two MATN3 mutants were compared to their isogenic controls to determine the effects of each mutation on the unfolded protein response.
2020-05-20 | GSE148728 | GEO
Project description:We set out to determine the role of the IRE1/XBP1 pathway, the most ancient and highly conserved endoplasmic reticulum (ER) stress-sensing pathway of the unfolded protein response (UPR), in Schmid metaphyseal chondrodysplasia (MCDS). RNA derived from hypertrophic zones microdissected from growth plates of wildtype mice, mice lacking XBP1 activity in chondrocytes (Xbp1Cart?Ex2), mice carrying a COL10A1 pN617K mutation (ColXN617K), and compound mutants (C/X) was analyzed by whole genome microarray analysis. 1633 probes were differentially expressed between ColXN617K and wildtype, 215 probes were differentially expressed between Xbp1Cart?Ex2 and wildtype, and 1337 probes were differentially expressed between C/X and wildtype. 885 probes were differentially expressed between ColXN617K and wildtype but not Xbp1Cart?Ex2 and wildtype or C/X and wildtype, thus representing the XBP1-dependent response to hypertrophic chondrocyte ER stress. 688 probes were differentially expressed between ColXN617K and wildtype and between C/X and wildtype but not Xbp1Cart?Ex2 and wildtype, thus representing the XBP1-independent response to hypertrophic chondrocyte ER stress. Results were validated by qPCR. Entire growth plate hypertrophic zones were microdissected from one tibia from each of three 2-week old wildtype mice, three 2-week old mice carrying a COL10A1 p.N617K mutation (ColXN617K), three 2-week old mice lacking XBP1 activity in chondrocytes (Xbp1Cart?Ex2), and three 2-week old mice resulting from a cross between ColXN617K and Xbp1Cart?Ex2 (C/X).
2015-08-21 | E-GEOD-72261 | biostudies-arrayexpress
Project description:Frozen blocks of human embryonic limb tissue were sectioned and laser capture microdissected to collect three human chodrocyte tissues - precursor, differentiated and hypertrophic chondrocytes.Total RNA including miRNAs was isolated and analyzed using Applied Biosystems OpenArrayM-BM-. Real-Time PCR system. RT-PCR miRNA expression profiling. miRNA expression from three chondrocyte sub types - precursor, differentiated and hypertrophic chondrocytes were analyzed using TaqManM-BM-. OpenArrayM-BM-. Human MicroRNA Panel.
2013-10-23 | E-GEOD-49152 | biostudies-arrayexpress
Project description:A comprehensive analysis of Sox9 binding profiles in developing chondrocytes identified marked enrichment of an AP-1-like motif (Ohba et al. 2015). Here, we have explored the functional interplay between Sox9 and AP-1 in mammalian chondrocyte development. Among AP-1 family members, Jun and Fosl2 were highly expressed within prehypertrophic and early hypertrophic chondrocytes. Chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) showed a striking overlap in Jun- and Sox9-bound regions throughout the chondrocyte genome, a reflection of direct binding of each factor to target motifs in shared enhancers, and physical interactions of AP-1 with Sox9. In vitro expression analysis indicates that direct co-binding of Sox9 and AP-1 at target motifs enhanced target gene expression, while protein-protein interactions suppressed AP-1- and Sox9-driven transcription. Analysis of prehypertrophic chondrocyte removal of Sox9 demonstrated Sox9 was essential for hypertrophic chondrocyte development, while in vitro and ex vivo analyses showed AP-1 promotes chondrocyte hypertrophy. Sox9 and Jun co-bound and co-activated a Col10a1 enhancer in Sox9 and AP-1 motif-dependent manners consistent with their combined action promoting hypertrophic gene expression. Together, the data support a model where AP-1-family members promote Sox9-action in the transition of chondrocytes to a terminal hypertrophic program. Intersection of ChIP-seq data from Sox9 and AP-1 factor Jun, RNA-seq data from developing rib chondrocytes and Col10a1mCherry positive hypertrophic chondrocytes in neonatal mice to uncover regulation of Sox9 by AP-1 factors during chondrocyte hypertrophy.
2016-02-29 | E-GEOD-73372 | biostudies-arrayexpress
Project description:We set out to determine the role of the IRE1/XBP1 pathway, the most ancient and highly conserved endoplasmic reticulum (ER) stress-sensing pathway of the unfolded protein response (UPR), in Schmid metaphyseal chondrodysplasia (MCDS). RNA derived from hypertrophic zones microdissected from growth plates of wildtype mice, mice lacking XBP1 activity in chondrocytes (Xbp1CartΔEx2), mice carrying a COL10A1 pN617K mutation (ColXN617K), and compound mutants (C/X) was analyzed by whole genome microarray analysis. 1633 probes were differentially expressed between ColXN617K and wildtype, 215 probes were differentially expressed between Xbp1CartΔEx2 and wildtype, and 1337 probes were differentially expressed between C/X and wildtype. 885 probes were differentially expressed between ColXN617K and wildtype but not Xbp1CartΔEx2 and wildtype or C/X and wildtype, thus representing the XBP1-dependent response to hypertrophic chondrocyte ER stress. 688 probes were differentially expressed between ColXN617K and wildtype and between C/X and wildtype but not Xbp1CartΔEx2 and wildtype, thus representing the XBP1-independent response to hypertrophic chondrocyte ER stress. Results were validated by qPCR.
2015-08-21 | GSE72261 | GEO
Project description:A comprehensive analysis of Sox9 binding profiles in developing chondrocytes identified marked enrichment of an AP-1-like motif (Ohba et al. 2015). Here, we have explored the functional interplay between Sox9 and AP-1 in mammalian chondrocyte development. Among AP-1 family members, Jun and Fosl2 were highly expressed within prehypertrophic and early hypertrophic chondrocytes. Chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) showed a striking overlap in Jun- and Sox9-bound regions throughout the chondrocyte genome, a reflection of direct binding of each factor to target motifs in shared enhancers, and physical interactions of AP-1 with Sox9. In vitro expression analysis indicates that direct co-binding of Sox9 and AP-1 at target motifs enhanced target gene expression, while protein-protein interactions suppressed AP-1- and Sox9-driven transcription. Analysis of prehypertrophic chondrocyte removal of Sox9 demonstrated Sox9 was essential for hypertrophic chondrocyte development, while in vitro and ex vivo analyses showed AP-1 promotes chondrocyte hypertrophy. Sox9 and Jun co-bound and co-activated a Col10a1 enhancer in Sox9 and AP-1 motif-dependent manners consistent with their combined action promoting hypertrophic gene expression. Together, the data support a model where AP-1-family members promote Sox9-action in the transition of chondrocytes to a terminal hypertrophic program.
2016-02-29 | GSE73372 | GEO
Project description:To survey altered gene expreesion in round, colmnar and hypertrophic chondrocytes of Tric-b-KO mice, total RNA preparations from round chondrocytes and colmnar/hypertrophic chondrocytes were subjected to gene microarray analysis. Results provide insight into the transcriptional profile of each Tric-b-KO chondrocyte and provide further insight into their functions.
2023-01-31 | GSE223776 | GEO
Project description:BACKGROUND: During osteoarthritis (OA), articular chondrocytes undergo phenotypic changes that resemble developmental patterns characteristic of growth plate chondrocytes. These phenotypic alterations lead to a hypertrophy-like phenotype characterized by altered production of extracellular matrix constituents and increased collagenase activity, which in turn results in cartilage destruction in OA disease. PURPOSE: To identify transcriptomic and epigenomic changes in murine primary articular chondrocytes undergoing hypertrophy-like differentiation in vitro. METHODS: We paired an in vitro 3D/pellet culture system that mimics chondrocyte hypertrophy with RNA sequencing (RNA-Seq) and enhanced reduced representation of bisulfite sequencing (ERRBS). RESULTS: We identified hypertrophy-associated changes in DNA methylation patterns in vitro. Integration of RNA-Seq and ERRBS datasets identified associations between changes in methylation and gene expression. CONCLUSION: Our integrative analyses showed that hypertrophic differentiation of articular chondrocytes is accompanied by transcriptomic and epigenomic changes in vitro.
2020-10-01 | GSE154949 | GEO