Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Skeletal dysplasia-causing TRPV4 mutations suppress the hypertrophic differentiation of human iPSC-derived chondrocytes

ABSTRACT: Skeletal dysplasia-causing TRPV4 mutations suppress the hypertrophic differentiation of human iPSC-derived chondrocytes

PROVIDER: PRJNA935718 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23498518_1.fastq.gz	Fastqsanger.gz
	SRR23498518_2.fastq.gz	Fastqsanger.gz
	SRR23498519_1.fastq.gz	Fastqsanger.gz
	SRR23498519_2.fastq.gz	Fastqsanger.gz
	SRR23498520_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 62

Similar Datasets

Skeletal dysplasia-causing TRPV4 mutations suppress the hypertrophic differentiation of human iPSC-derived chondrocytes

Project description:To elucidate how TRPV4 mutations cause skeletal dysplasia, we used CRISPR-Cas9-edited hiPSCs harboring the moderate V620I and lethal T89I mutations to differentiate chondrocytes and hypertrophic chondrocytes. We then used mRNA sequencing to analyze differential gene expression between 3 cell lines, 2 time points, and 2 treatments.

2023-02-16 | GSE225446 | GEO

Skeletal dysplasia-causing TRPV4 mutations suppress the hypertrophic differentiation of human iPSC-derived chondrocytes.

Project description:Mutations in the TRPV4 ion channel can lead to a range of skeletal dysplasias. However, the mechanisms by which TRPV4 mutations lead to distinct disease severity remain unknown. Here, we use CRISPR-Cas9-edited human-induced pluripotent stem cells (hiPSCs) harboring either the mild V620I or lethal T89I mutations to elucidate the differential effects on channel function and chondrogenic differentiation. We found that hiPSC-derived chondrocytes with the V620I mutation exhibited increased basal currents through TRPV4. However, both mutations showed more rapid calcium signaling with a reduced overall magnitude in response to TRPV4 agonist GSK1016790A compared to wildtype (WT). There were no differences in overall cartilaginous matrix production, but the V620I mutation resulted in reduced mechanical properties of cartilage matrix later in chondrogenesis. mRNA sequencing revealed that both mutations up-regulated several anterior HOX genes and down-regulated antioxidant genes CAT and GSTA1 throughout chondrogenesis. BMP4 treatment up-regulated several essential hypertrophic genes in WT chondrocytes; however, this hypertrophic maturation response was inhibited in mutant chondrocytes. These results indicate that the TRPV4 mutations alter BMP signaling in chondrocytes and prevent proper chondrocyte hypertrophy, as a potential mechanism for dysfunctional skeletal development. Our findings provide potential therapeutic targets for developing treatments for TRPV4-mediated skeletal dysplasias.

| S-EPMC9949800 | biostudies-literature

Transcription profiling of chicken proliferative and hypertrophic chondrocytes

Project description:Longitudinal bone growth depends upon the execution of an intricate series of cellular activities by epiphyseal growth plate chondrocytes. In order to better understand these coordinated events, microarray analysis was used to compare gene expression in chondrocytes isolated from the proliferative and hypertrophic zones of the avian growth plate. In this experiment we compared pooled samples of proliferative and hypertrophic chondrocytes isolated from the chick growth plate. The expression of 745 genes was found to differ 3-fold or greater at the 0.05 level of probability. Experiment Overall Design: We examined 8 samples using arrays: 4 from proliferative and 4 from hypertrophic chondrocytes.

2009-10-23 | E-GEOD-18568 | biostudies-arrayexpress

Round, columnar and hypertrophic chondrocytes of wild type mice

Project description:To survey altered gene expreesion in round, colmnar and hypertrophic chondrocytes of wil type 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 chondrocytes and provide further insight into their functions.

2018-10-31 | GSE105256 | GEO

Transcription profiling of Bos taurus hypertrophic growth plate chondrocytes vs. reserve zone chondrocytes

Project description:Growth plate chondrocytes were isolated from the distal metacarpus of young dairy cattle (all under 10 mo of age), the chondrocytes were released from the extracellular matrix by digestion with Collagenase P for 4 hours, and the various zones of the growth plate were separated by density centrifugation. The least-dense Hypertrophic Zone (HZ) cells were compared to the most-dense Reserve Zone (RZ) cells. 6 pairs of HZ vs RZ were compared by microarray. Experiment Overall Design: Growth plate chondrocytes were isolated from the distal metacarpus of young dairy cattle (all under 10 mo of age), the chondrocytes were released from the extracellular matrix by digestion with Collagenase P for 4 hours, and the various zones of the growth plate were separated by density centrifugation. The least-dense Hypertrophic Zone (HZ) cells were compared to the most-dense Reserve Zone (RZ) cells. Six independent sample pairs of HZ vs RZ were compared by microarray.

2009-10-30 | E-GEOD-18738 | biostudies-arrayexpress

Round or columnar and hypertrophic chondrocytes of Tric-b-KO mice

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

Bovine Hypertrophic Growth Plate Chondrocytes vs. Reserve Zone Chondrocytes

2009-10-27 | GSE18738 | GEO

Chondrocyte Gene Expression in Proliferative and Hypertrophic Chondrocytes of Chick

2009-10-16 | GSE18568 | GEO

Epigenetic mechanisms mediating the transition from proliferating into hypertrophic chondrocytes. [RNA-Seq]

Project description:Correlation of RNA-seq and ChIP-seq data from proliferating (PC) and hypertrophic chondrocytes (HC).

2021-03-10 | GSE155400 | GEO

Epigenetic mechanisms mediating the transition from proliferating into hypertrophic chondrocytes. [ChIP-Seq]

Project description:Chromatin Immunopreciptiation of histone modifications in primary proliferating (PC) and hypertrophic chondrocytes (HC) from embryonic mice

2021-03-10 | GSE155399 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data