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Gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes [scRNA-seq]

ABSTRACT: gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes [scRNA-seq]

PROVIDER: PRJNA764524 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15965269_1.fastq.gz	Fastqsanger.gz
	SRR15965269_2.fastq.gz	Fastqsanger.gz
	SRR15965270_1.fastq.gz	Fastqsanger.gz
	SRR15965270_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes

Project description:gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes

| PRJNA778522 | ENA

gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes [bulkRNA-seq]

Project description:Growth of long bones and vertebrae is maintained postnatally by a long-lasting pool of progenitor cells. Little is known about the molecular mechanisms that regulate the output and maintenance of the cells that give rise to mature cartilage. Here we demonstrate that postnatal chondrocyte-specific deletion of a transcription factor Stat3 results in severely reduced proliferation coupled with increased hypertrophy, growth plate fusion, stunting and signs of progressive dysfunction of the articular cartilage. This effect is dimorphic, with females more strongly affected than males. Chondrocyte-specific deletion of the IL-6 family cytokine receptor gp130, which activates Stat3, phenocopied Stat3-deletion; deletion of Lifr, one of many co-receptors that signals through gp130, resulted in a milder phenotype. These data define a new molecular circuit that regulates chondrogenic cell maintenance and output and reveals a novel, hitherto unrecognized function of IL-6 cytokines in the skeletal system with direct implications for skeletal development and regeneration.

2022-02-08 | GSE188353 | GEO

gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes [scRNA-seq]

2022-02-08 | GSE184406 | GEO

gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes [bulkRNA-seq]

Project description:gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes [bulkRNA-seq]

| PRJNA778523 | ENA

gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes.

Project description:Growth of long bones and vertebrae is maintained postnatally by a long-lasting pool of progenitor cells. Little is known about the molecular mechanisms that regulate the output and maintenance of the cells that give rise to mature cartilage. Here we demonstrate that postnatal chondrocyte-specific deletion of a transcription factor Stat3 results in severely reduced proliferation coupled with increased hypertrophy, growth plate fusion, stunting and signs of progressive dysfunction of the articular cartilage. This effect is dimorphic, with females more strongly affected than males. Chondrocyte-specific deletion of the IL-6 family cytokine receptor gp130, which activates Stat3, phenocopied Stat3-deletion; deletion of Lifr, one of many co-receptors that signals through gp130, resulted in a milder phenotype. These data define a molecular circuit that regulates chondrogenic cell maintenance and output and reveals a pivotal positive function of IL-6 family cytokines in the skeletal system with direct implications for skeletal development and regeneration.

| S-EPMC8763901 | biostudies-literature

gp130/STAT3 signaling is required for homeostatic proliferation and anabolism in postnatal growth plate and articular chondrocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-02-08 | GSE188354 | GEO

Bulk RNA-seq of articular and growth plate chondrocytes from control and Sox9 mutant mice

Project description:Using a conditional inactivation approach in the mouse, we examined the importance of SOX9 in adult growth plate and articular cartilage. We specifically investigated the roles of SOX9 in the expression of the pancartilaginous, growth-plate and articular programs and in maintaining the chondrocyte lineage fate.

2021-02-19 | GSE154381 | GEO

RNA-seq data from mouse articular chondrocytes

Project description:To understand the effect of semaphorin 4D on articular chondrocytes, articular chondrocytes were stimulated with semaphorin 4D. Total RNA was analyzed by RNA-seq.

2022-11-01 | GSE167852 | GEO

Expression data from articular and growth plate cartilage

Project description:The aim of the current study was to identify molecular markers for articular cartilage that can be used for the quality control of tissue engineered cartilage. Therefore a genom-wide expression analysis was performed using RNA isolated from articular and growth plate cartilage, both extracted from the knee joints of minipigs. Keywords: Native material or primary cells isolated from articular cartilage and growth plate cartilage

2011-07-29 | GSE23492 | GEO

Gene expression profiling of tankyrase-inhibited mouse articular chondrocytes

Project description:Osteoarthritis (OA) is a prevalent degenerative disease, which involves progressive and irreversible destruction of cartilage matrix. Despite efforts to reconstruct cartilage matrix in osteoarthritic joints, it has been a difficult task as adult cartilage exhibits marginal repair capacity. Here we report the identification of tankyrase as a regulator of the cartilage anabolism axis based on systems-level factor analysis of mouse reference populations. Tankyrase inhibition drives the expression of a cartilage-signature matrisome and elicits a transcriptomic pattern that is inversely correlated with OA progression. Furthermore, tankyrase inhibitors ameliorate surgically-induced OA in mice, and stem cell transplantation coupled with tankyrase knockdown results in superior regeneration of cartilage lesions. Mechanistically, the pro-regenerative features of tankyrase inhibition are mainly triggered by uncoupling SOX9 from a poly(ADP-ribosyl)ation (PARylation)-dependent protein degradation pathway. Our findings provide insights into the development of future OA therapies aimed at reconstruction of articular cartilage.

2019-09-24 | GSE137899 | GEO

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