Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression in degenerated rat supraspinatus tendon

ABSTRACT: Microarray of exercised (degenerated) rat supraspinatus versus non-exercised (normal) rats were subjected to exercise that consisted of running on a 10Ë decline at 17m/min for 1 hour per day, 5 days per week. This regimen equates to approximately 7500 strides per day. After four weeks of running, rats were sacrificed by CO2 inhalation and both supraspinatus tendons were collected. 12 non-exercised rats were used as controls.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Tim Molloy

PROVIDER: E-GEOD-4575 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Microarray analysis of the tendinopathic rat supraspinatus tendon: glutamate signaling and its potential role in tendon degeneration.

Molloy T J TJ Kemp M W MW Wang Y Y Murrell G A C GA

Journal of applied physiology (Bethesda, Md. : 1985) 20060803 6

Degenerative tendon injury or "tendinopathy" is one of the most common disorders of the musculoskeletal system. We used a rat model (Soslowsky LJ, Thomopoulos S, Tun S, Flanagan CL, Keefer CC, Mastaw J, and Carpenter JE. J Shoulder Elbow Surg 9: 79-84, 2000) to identify novel gene expression in the exercised-induced degenerated supraspinatus tendon by microarray and real-time PCR analyses. We identified several novel groups of differentially expressed genes, including those involved in apoptosis ...[more]

PMID: 16888051

Similar Datasets

Gene expression in degenerated rat supraspinatus tendon

Project description:Microarray of exercised (degenerated) rat supraspinatus versus non-exercised (normal) Keywords: Disease state analysis

2006-06-21 | GSE4575 | GEO

Prostaglandin D2 Signaling in Tendon Healing

Project description:We report RNA sequencing data from the plantaris tendons of 3-month old Sprague Dawley rats that were treated with vehicle or GSK2894631A to inhibit the HPGDS enzyme. Rats underwent a bilateral plantaris tendon tear followed by immediate repair, and samples were obtained either 7 or 21 days after surgical intervention.

2019-09-20 | GSE130276 | GEO

Transcriptomic signatures of exercised tendon in male rats

Project description:Transcriptomic signatures of exercised tendon in male rats

| PRJEB30778 | ENA

Transcriptomic signatures of exercised tendon in male rats

Project description:Six rats (treatment group) underwent a 13-week downhill treadmill running exercise programme and six rats (control group) were studied in this experiments. The RNAs were extracted from rat Achille's tendon tissue and sequenced using Illumina Hiseq platform.

2020-06-30 | E-MTAB-7563 | biostudies-arrayexpress

Tenomodulin prevents trauma-induced heterotopic ossification in tendon

Project description:We have reported that loss of Tnmd leads to inferior early tendon repair characterized by fibrovascular scaring and therefore hypothesized that its lack will persistently cause deficient repair during later stages. Tnmd knockout (Tnmd-/-) and wild-type (WT) animals were subjected to complete Achilles tendon surgical transection followed by end-to-end suture. Lineage tracing revealed a reduction in tendon-lineage cells marked by ScleraxisGFP, but an increase in alpha smooth muscle actin myofibroblasts in Tnmd-/- tendon scars. At the proliferative stage, more pro-inflammatory M1 macrophages and larger collagen II cartilaginous template were detected in this group. At the remodeling stage, histological scoring revealed lower repair quality in the injured Tnmd-/- tendons, which was coupled with higher HO quantified by micro-CT. Tendon biomechanical properties were compromised in both groups upon injury, however we identified an abnormal stiffening of non-injured Tnmd-/- tendons, which possessed higher static and dynamic E-moduli. Pathologically thicker and abnormally shaped collagen fibrils were observed by TEM in Tnmd-/- tendons and this together with augmented HO resulted in diminished running capacity of Tnmd-/- mice. These novel findings demonstrate that Tnmd plays a protecting role against trauma-induced endochondral HO and can inspire the generation of novel therapeutics to accelerate repair.

2021-11-08 | GSE179454 | 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

Myocardial proteome changes in aortic stenosis rats subjected to long-term aerobic exercise

Project description:The effects of exercise training (ET) on the heart of aortic stenosis (AS) rats are controversial and the mechanisms involved in alterations induced by ET have been poorly clarified. In this study we analyzed the myocardial proteome to identify proteins modulated by moderate intensity aerobic ET in rats with chronic supravalvar AS. Wistar rats were divided into four groups: sedentary control (C-Sed), exercised control (C-Ex), sedentary aortic stenosis (AS-Sed), and exercised AS (AS-Ex). ET consisted of five treadmill running sessions per week for 16 weeks. Statistical analysis was performed by ANOVA or Kruskal-Wallis and Goodman tests. Results were discussed at a significance level of 5%. At the end of the experiment, AS-Ex rats had higher functional capacity, lower blood lactate concentration, and better cardiac structural and left ventricular functional parameters than the AS-Sed. Myocardial proteome analysis showed that AS-Sed had higher protein expressions related to the glycolytic pathway, oxidative stress, and inflammation, and lower protein expressions related to beta-oxidation than C-Sed. AS-Ex had higher expression of one protein related to mitochondrial biogenesis and lower protein expressions associated with oxidative stress and inflammation than AS-Sed. Proteomic data were validated for proteins related to lipid and glycolytic metabolism. In conclusion, chronic pressure overload changes the expression of myocardial proteins that are mainly involved in lipid and glycolytic energy metabolism in rats. Moderate intensity aerobic training attenuates protein expressions related to oxidative stress and inflammation and increases protein expressions related to mitochondrial biogenesis. Protein changes are associated with improved functional capacity, cardiac remodeling and left ventricular function in aortic stenosis rats.

2024-02-29 | PXD040785 | Pride

RNA-Seq analysis to study the transcriptomic profiles of mice after 4-month wheel running exercise

Project description:To identify the mechanism underlying AdipoR1-mediated beneficial effect of exercise, we used RNA-Seq analysis to study the transcriptomic profiles of mice after 4-month wheel running exercise. Differential expression analysis was performed by comparing exercised mice to control mice, and exercised mice subjected to AdipoR1 shRNA versus exercised mice.

2022-09-26 | GSE205019 | GEO

Prim-O-glucosylcimifugin ameliorates aging-impaired endogenous tendon regeneration capacity via rejuvenating senescent tendon stem/progenitor cells [DMSO-treated and POG-treated TSPCs]

Project description:Adult tendon stem/progenitor cells (TSPCs) are essential for tendon maintenance, regeneration, and repair, yet they become susceptible to senescence with age, impairing the self-healing capacity of tendons. In this study, we employ a recently developed deep-learning-based efficacy prediction system to screen potential stemness-promoting and senescence-inhibiting drugs from natural products using the transcriptional signatures of stemness. The top-ranked candidate prim-O-glucosylcimifugin (POG), a saposhnikovia root extract, could ameliorate TPSC- senescent phenotypes caused by long-term passage and natural aging in rats and humans, as well as restore self-renewal and proliferation capacities, and tenogenic potential of aged TSPCs. In vivo, the systematic administration of POG or the local delivery of POG nanoparticles functionally rescues endogenous tendon regeneration and repair capacity in aged rats to levels similar to normal animals. Mechanistically, POG protects TSPCs against functional impairment during both passage-induced and natural aging by simultaneously suppressing nuclear factor-κB and downregulating mTOR signaling with induction of autophagy. Together, the strategy by pharmacological intervention with deep learning-predicted compound POG could rejuvenate aged TSPCs and improve the regenerative capacity of aged tendons. We performed mRNA microarray analyses of DMSO-treated and POG-treated TSPCs from 18-month-old rats and identified meaningful genes in down-regulated and up-regulated group

2023-11-02 | GSE241202 | GEO

Prim-O-glucosylcimifugin ameliorates aging-impaired endogenous tendon regeneration capacity via rejuvenating senescent tendon stem/progenitor cells [DMSO-treated and POG-treated Passage 12 TSPCs]

Project description:Adult tendon stem/progenitor cells (TSPCs) are essential for tendon maintenance, regeneration, and repair, yet they become susceptible to senescence with age, impairing the self-healing capacity of tendons. In this study, we employ a recently developed deep-learning-based efficacy prediction system to screen potential stemness-promoting and senescence-inhibiting drugs from natural products using the transcriptional signatures of stemness. The top-ranked candidate prim-O-glucosylcimifugin (POG), a saposhnikovia root extract, could ameliorate TPSC- senescent phenotypes caused by long-term passage and natural aging in rats and humans, as well as restore self-renewal and proliferation capacities, and tenogenic potential of aged TSPCs. In vivo, the systematic administration of POG or the local delivery of POG nanoparticles functionally rescues endogenous tendon regeneration and repair capacity in aged rats to levels similar to normal animals. Mechanistically, POG protects TSPCs against functional impairment during both passage-induced and natural aging by simultaneously suppressing nuclear factor-κB and downregulating mTOR signaling with induction of autophagy. Together, the strategy by pharmacological intervention with deep learning-predicted compound POG could rejuvenate aged TSPCs and improve the regenerative capacity of aged tendons. We performed mRNA microarray analyses of DMSO-treated and POG-treated Passage 12 TSPCs and identified meaningful genes in down-regulated and up-regulated group

2023-11-02 | GSE241201 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data