Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA318791 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3400471_1.fastq.gz | Fastqsanger.gz | |||
| SRR3400471_2.fastq.gz | Fastqsanger.gz | |||
| SRR3400472_1.fastq.gz | Fastqsanger.gz | |||
| SRR3400472_2.fastq.gz | Fastqsanger.gz | |||
| SRR3400473_1.fastq.gz | Fastqsanger.gz |
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Project description:We partnered with Zymo Research, Inc. to detect genome-wide methylation changes associated with the initiation and progression of tendinopathy induced by TGF-β1 in a murine Achilles tendon model. All genes identified as significantly differentially methylated were present in only one experimental group showing that both the gene identified and its modified methylation status are dependent on the injury time-course and activity level. In summary, we identified five genes (Leprel2, Foxf1, Mmp25, Igfbp6 and Peg12) which demonstrate significant relevance to tendon biology with three exhibiting functions in collagen fibril organization. We postulate that a study of the molecular genomics of these genes in animal and human tendon could further delineate the pathogenesis of this multifactorial disease.
2016-08-17 | GSE80396 | GEO
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
Project description:Achilles tendinopathy is often thought to be a consequence of overuse of the Cells within the Achilles tendon of healthy rats undergo a series of changes following physiologic levels of mechanical stimulation after running, and we further explored the transcriptome changes in Achilles tendon cells during post-exercise recovery. Our current experiment reveals RNA-seq analysis of the transcriptome of the rat Achilles tendon after 12 hours of rest following running.
2024-10-07 | GSE270400 | 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: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.
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Project description:Tendon is a highly aligned connective tissue, in which the macro-structure consists of collagen-rich fascicles surrounded by interfascicular matrix (IFM). In a series of recent studies in equine tissue, we have demonstrated specialisation of tendon composition, structure and mechanics to achieve the tendon’s functional requirements, specifically reporting extensive specialisation of the IFM region in the energy storing superficial digital flexor tendon. We have also demonstrated loss of functional specialisms with ageing, leading to a hypothesised new paradigm for tendinopathy, focused on the importance of the IFM. However, to date, there have been no studies focused on structure-function specialisation or the IFM in functionally distinct human tendons. Here, we compare the positional anterior tibialis tendon and energy storing Achilles tendon, performing a detailed analysis of the composition and mechanical properties of both fascicle and IFM regions, to test the hypothesis that the IFM in the energy storing Achilles tendon has specialised composition and mechanical properties, and that these specialisations are lost with ageing. We demonstrate that the IFM is specialised in the energy storing Achilles tendon, with greater elasticity and fatigue resistance than in the positional anterior tibialis tendon. While there were few age-related alterations in mechanics, we did identify age-related alterations in the IFM proteome of the Achilles tendon specifically, which is predicted to be regulated by TGF-beta signalling and may be responsible for the trend towards decreased fatigue resistance observed in the Achilles IFM with ageing.
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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:It has previously been reported that expression levels of insulin-like growth factor binding protein 6 (IGFBP6) are reduced in unstable plaques compared to stable plaques in patients with coronary heart disease (CAD). However, the exact role and mechanism of IGFBP6 in endothelial homeostasis and inhibition of focal atherosclerotic plaque development in vivo remains unclear. Transcripome sequencing and bioinformatics analysis of IGFBP6-overexpressed human umbilical vein endothelial cells (HUVECs) suggest that pathway analysis and differentially expressed mRNA may help clarify the role and potential mechanism of IGFBP6 in the treatment of cardiovascular diseases.
2024-05-01 | GSE265787 | GEO
Project description:FOXF1, a member of the forkhead box family of transcription factors, has been previously shown to be critical for lung development, homeostasis, and injury responses. However, the role of FOXF1 in lung regeneration is unknown. Herein, we performed partial pneumonectomy, a model of lung regeneration, in mice lacking one Foxf1 allele in endothelial cells (PDGFb-iCre/Foxf1fl/+ mice). Endothelial cell proliferation was significantly reduced in regenerating lungs from mice deficient for endothelial Foxf1. Decreased endothelial proliferation was associated with delayed lung regeneration as shown by reduced respiratory volume in Foxf1-deficient lungs. FACS-sorted endothelial cells isolated from regenerating PDGFb-iCre/Foxf1fl/+ and control lungs were used for RNAseq analysis to identify FOXF1 target genes. Foxf1 deficiency altered expression of numerous genes including those regulating extracellular matrix remodeling (Timp3, Adamts9) and cell cycle progression (Cdkn1a, Cdkn2b, Cenpj, Tubb4a), which are critical for lung regeneration. Deletion of Foxf1 increased Timp3 mRNA and protein, decreasing MMP14 activity in regenerating lungs. ChIPseq analysis for FOXF1 and histone methylation marks identified DNA regulatory regions with the Cd44, Cdkn1a, and Cdkn2b genes, indicating they are direct FOXF1 targets. Thus FOXF1 stimulates lung regeneration following partial pneumonectomy via direct transcriptional regulation of genes critical for extracellular matrix remodeling and cell cycle progression.
2017-09-12 | GSE100149 | 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.
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