Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1283482 | ENA |
REPOSITORIES: ENA
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Project description:RNA-seq of topical Notoginsenoside R1(NR1) and berberine treatment on diabetic ulcers
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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 | GSE181172 | GEO
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
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
Project description:Tendinopathy is characterized by rupture, pain, or loss of tendon strength. Previous basic and clinical investigations have clarified multiple risk factors, including aging and fluoroquinolone use; however, the etiology remains unclear. We combined real-world data analysis with pharmacological experiments to overcome the gap between basic and clinical research. Analyses of self-reported adverse event databases and the US commercial claims database revealed that dexamethasone prevented fluoroquinolone-induced and age-related tendinopathy. Experimental validation suggested that co-treatment with dexamethasone attenuated pefloxacin-induced mechanical fragility in rat tendons. RNA-seq was conducted to further investigate the molecular mechanism of tendinopathy, focusing on fluoroquinolone.
2023-04-12 | GSE212344 | GEO
Project description:Tendinopathy is a common disease of the musculoskeletal system, however, the mechanism of tendinopathy has not yet been elucidated, and there are no clear conclusions about the changes in gene expression within tendinopathy. In order to better investigate the mechanisms inherent to the development of tendinopathy, we performed RNA sequencing on normal tendon cells and inflammatory tendon cells
2024-02-05 | GSE253913 | GEO
Project description:Tendinopathy is a common disease in individuals whose tendons suffer from repetitive strains, such as athletes. The lack of knowledge regarding the pathological mechanisms causes inadequate prevention methods and low cure rate of this disease. Repetitive strain injury is thought to be the source of tendinopathy; therefore, we investigate the effect of mechanical loading on tendon and seek the ways to prevent and treat tendinopathy better. In our study, we found that the expression of a mechanosensitive miRNA, miR-337-3p, decreased in tendon-derived stem cells (TDSCs) under uniaxial cyclical mechanical loading with 10% elongation. In addition, miR-337-3p was negatively related to chondro-osteogenic differentiation of TDSCs, in which lower expression was found in human calcified tendons and rat tendinopathy samples.
2018-05-24 | GSE114828 | GEO
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.
2011-06-07 | GSE26051 | GEO
Project description:As people become more motivated to exercise regularly and stay healthy, tendinopathy is a common problem in both active athletes and inactive individuals, which imposes a considerable social and economic burden. Here we provide a single-cell multi-modal ATAC + gene expression sequencing in tendinopathy. We have identified pathways and genes regulated in tendinopathy samples that will help contribute to further investigation into the development and molecular hallmarks of tendinopathy.
2023-05-31 | GSE213803 | GEO