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Il-6 signaling exacerbates hallmarks of tendon lesions by stimulating progenitor proliferation & migration to damage.

ABSTRACT: Il-6 signaling exacerbates hallmarks of tendon lesions by stimulating progenitor proliferation & migration to damage.

PROVIDER: PRJNA883640 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21683458.fastq.gz	Fastqsanger.gz
	SRR21683459.fastq.gz	Fastqsanger.gz
	SRR21683460.fastq.gz	Fastqsanger.gz
	SRR21683461.fastq.gz	Fastqsanger.gz
	SRR21683462.fastq.gz	Fastqsanger.gz

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Il-6 signaling exacerbates hallmarks of tendon lesions by stimulating progenitor proliferation & migration to damage.

Project description:We leveraged an explant-based, tissue engineered model of tendon damage to study cross-compartmental interactions between the tendon core and extrinsic progenitors, as well as between the tendon core and extrinsic macrophages. We suspected IL-6 signaling to play a major role in this crosstalk, so we also incorporated core explants from IL-6 knock-out mice.

2023-09-13 | GSE214015 | GEO

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]

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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

Tendon injury

Project description:Tendon injury

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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 [seq]

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

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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

RNA-seq of achilles tendon from young and old donors to study age-related changes in tendon

Project description:Tendon from young and old donors was used for RNA-Seq analysis. The aim of the study was to identify differentially expressed tendon transcripts in ageing in order to to characterize molecular mechanisms associated with age-related changes in tendon.

2015-04-01 | E-MTAB-2449 | biostudies-arrayexpress

Angiopoietin-like 4 enhances the ability of tendon fibroblasts to undergo proliferation and migration

Project description:This microarray study provides novel insights into the role of Angiopoietin-like 4 in tendon biology with implications for injury repair and exercise physiology.

2016-04-17 | GSE80356 | GEO

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