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CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition [seq]

ABSTRACT: CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition [seq]

PROVIDER: PRJNA750927 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15305073_1.fastq.gz	Fastqsanger.gz
	SRR15305073_2.fastq.gz	Fastqsanger.gz
	SRR15305074_1.fastq.gz	Fastqsanger.gz
	SRR15305074_2.fastq.gz	Fastqsanger.gz
	SRR15305075_1.fastq.gz	Fastqsanger.gz

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CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition

Project description:CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition

| PRJNA750924 | ENA

CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition [array]

Project description:Tendinopathy, the most common disorder affecting tendons, is characterized by chronic disorganization of the tendon matrix, which eventually leads to tendon tear and rupture. The goal of this study was to identify a rational molecular target whose blockade can serve as a potential therapeutic intervention for tendinopathy. We identified C1q/TNF-related protein-3 (CTRP3) as a markedly upregulated cytokine in human and rodent tendinopathy. Overexpression of CTRP3 enhanced the progression of tendinopathy by accumulating cartilaginous proteoglycans and degenerating collagenous fibers in the mouse tendon, whereas CTRP3 knockdown suppressed the tendinopathy pathogenesis. Functional blockade of CTRP3 using a neutralizing antibody ameliorated overuse-induced tendinopathy of the Achilles and rotator cuff tendons. Mechanistically, CTRP3 elicited a transcriptomic pattern that stimulates abnormal differentiation of tendon stem/progenitor cells (TSPCs) and ectopic chondrification in tendons, as an effect linked to activation of Akt signaling. Collectively, we reveal an essential role for CTRP3 in tendinopathy and propose a potential therapeutic strategy for the treatment of tendinopathy.

2021-10-02 | GSE180368 | GEO

CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition [seq]

2021-10-02 | GSE181172 | GEO

CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition [array]

Project description:CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition [array]

| PRJNA748021 | ENA

CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition.

Project description:[Figure: see text].

| S-EPMC8604415 | biostudies-literature

CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition

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

2021-10-02 | GSE181173 | GEO

Analysis of Human Tendinopathy Gene Expression

Project description:Chronic tendon injuries, also known as tendinopathy, are common among professional and recreational athletes. These injuries result in a significant amount of morbidity and health care expenditure and yet little is known about the molecular mechanism leading to tendinopathy. We have used histological evaluation and molecular profiling to determine the gene expression changes in 23 human patients undergoing surgical procedures for the treatment of chronic tendinopathy. Diseased tendons have altered extracellular matrix, fiber disorientation, increased cellular content and vasculature and the absence of inflammatory cells. Global gene expression profiling identified 1783 transcripts with significant different expression patterns in the diseased tendons. Global pathway analysis further suggests altered expression of extracellular matrix proteins and the lack of an appreciable inflammatory response. We have identified pathways and genes regulated in tendinopathy samples that will help contribute to the understanding of the disease towards the development of novel therapeutics. A prospective study was initiated to collect tissue from patients undergoing surgery as standard of care for tendinopathy. Biopsies (~3mm^3) of diseased tendons as well as a section of grossly normal appearing tendon were collected from 23 patients. Written informed consent was obtained from all patients prior to any study related procedure.

2011-06-07 | E-GEOD-26051 | biostudies-arrayexpress

Analysis of Human Tendinopathy Gene Expression

2011-06-07 | GSE26051 | GEO

Single-cell transcriptomic profiling reveals distinct mechanical responses between normal and diseased tendon progenitor cells

Project description:Regenerative medicine approaches utilizing stem cells offer a promising strategy to address tendinopathy, a class of common tendon disorders associated with pain and impaired function. Tendon progenitor cells (TPCs) are important in healing and maintaining tendon tissues. Here we provide a comprehensive single cell transcriptomic profiling of TPCs from three normal and three clinically classified tendinopathy samples in response to mechanical stimuli. Analysis reveals seven distinct TPC subpopulations including subsets that are responsive to the mechanical stress, highly clonogenic, and specialized in cytokine or growth factor expression. The single cell transcriptomic profiling of TPCs and their subsets serves as a foundation for further investigation into the pathology and molecular hallmarks of tendinopathy in mechanical stimulation conditions.

2021-07-07 | GSE150482 | GEO

Effects of running for 1h on gene expression in Achilles tendon cells of SD rats

Project description:The Achilles tendon is the thickest tendon in the human body, and Achilles tendinopathy is its most prevalent disorder, often considered a consequence of overuse. While disruption to the collagen fibers represents a significant manifestation of Achilles tendinopathy, strikingly little is known about the mechanisms by which healthy tendon accumulates damage in vivo.As existing studies of tendon biomechanics and mechanobiology predominantly relied on in vitro or ex vivo experiments on isolated tissues, it is still largely unknown whether and how disruptions occur to the collagen molecules in healthy Achilles tendons following physiological activities. We reported the first RNA-seq analysis reflecting transcriptome changes in healthy rat Achilles tendons following running, providing a resource for future investigations in tendon mechanobiology and sports medicine.

2024-10-07 | GSE269529 | GEO

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