Gene expression in degenerated rat supraspinatus tendon
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE4575 | GEO | 2006/06/21
SECONDARY ACCESSION(S): PRJNA94413
REPOSITORIES: GEO
Similar Datasets
Project description: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.
2010-07-01 | E-GEOD-4575 | biostudies-arrayexpress
Project description:Gene expression in degenerated rat supraspinatus tendon
| PRJNA94413 | ENA
Project description:Background: Low back pain is a leading cause of disability worldwide and is frequently attributed to intervertebral disc (IVD) degeneration. Though the contributions of the adjacent cartilage endplates (CEP) to IVD degeneration are well documented, the phenotype and functions of the resident CEP cells are critically understudied. To better characterize CEP cell phenotype and possible mechanisms of CEP degeneration, bulk and single-cell RNA-Sequencing of non-degenerated and degenerated CEP cells were performed. Methods: Human lumbar CEP cells from degenerated (Thompson Grade ≥ 4) and non-degenerated (Thompson Grade ≤ 2) discs were expanded for bulk (N=4 non-degenerated, N=4 degenerated) and single-cell (N=1 non-degenerated, N=1 degenerated) RNA-Sequencing. Genes identified from bulk RNA-Sequencing were categorized by function and their expression in non-degenerated and degenerated CEP cells were compared. A PubMed literature review was also performed to determine which genes were previously identified and studied in the CEP, IVD, and other cartilaginous tissues. For single-cell RNA-Sequencing, different cell clusters were resolved using unsupervised clustering and functional annotation. Differential gene expression analysis and Gene Ontology, respectively, were used to compare gene expression and functional enrichment between cell clusters, as well as between non-degenerated and degenerated CEP samples. Results: Bulk RNA-Sequencing revealed 38 genes were significantly upregulated and 15 genes were significantly downregulated in degenerated CEP cells relative to non-degenerated cells (|Fold change| ≥ 1.5). Of these, only 2 genes were previously studied in CEP cells and 31 were previously studied in the IVD and other cartilaginous tissues. Single-cell RNA-Sequencing revealed 11 unique cell clusters, including multiple chondrocyte and progenitor subpopulations with distinct gene expression and functional profiles. Analysis of genes in the bulk RNA-Sequencing dataset showed that progenitor cell clusters from both samples were enriched in “non-degenerated” genes, but not “degenerated” genes. For both bulk- and single-cell analyses, gene expression and pathway enrichment analyses highlighted several pathways that may regulate CEP degeneration, including transcriptional regulation, translational regulation, intracellular transport, and mitochondrial dysfunction. Conclusions: This thorough analysis using RNA-Sequencing methods highlighted numerous differences between non-degenerated and degenerated CEP cells, the phenotypic heterogeneity of CEP cells, and several pathways of interest that may be relevant in CEP degeneration.
2024-01-10 | GSE242040 | GEO
Project description:Background: Low back pain is a leading cause of disability worldwide and is frequently attributed to intervertebral disc (IVD) degeneration. Though the contributions of the adjacent cartilage endplates (CEP) to IVD degeneration are well documented, the phenotype and functions of the resident CEP cells are critically understudied. To better characterize CEP cell phenotype and possible mechanisms of CEP degeneration, bulk and single-cell RNA-Sequencing of non-degenerated and degenerated CEP cells were performed. Methods: Human lumbar CEP cells from degenerated (Thompson Grade ≥ 4) and non-degenerated (Thompson Grade ≤ 2) discs were expanded for bulk (N=4 non-degenerated, N=4 degenerated) and single-cell (N=1 non-degenerated, N=1 degenerated) RNA-Sequencing. Genes identified from bulk RNA-Sequencing were categorized by function and their expression in non-degenerated and degenerated CEP cells were compared. A PubMed literature review was also performed to determine which genes were previously identified and studied in the CEP, IVD, and other cartilaginous tissues. For single-cell RNA-Sequencing, different cell clusters were resolved using unsupervised clustering and functional annotation. Differential gene expression analysis and Gene Ontology, respectively, were used to compare gene expression and functional enrichment between cell clusters, as well as between non-degenerated and degenerated CEP samples. Results: Bulk RNA-Sequencing revealed 38 genes were significantly upregulated and 15 genes were significantly downregulated in degenerated CEP cells relative to non-degenerated cells (|Fold change| ≥ 1.5). Of these, only 2 genes were previously studied in CEP cells and 31 were previously studied in the IVD and other cartilaginous tissues. Single-cell RNA-Sequencing revealed 11 unique cell clusters, including multiple chondrocyte and progenitor subpopulations with distinct gene expression and functional profiles. Analysis of genes in the bulk RNA-Sequencing dataset showed that progenitor cell clusters from both samples were enriched in “non-degenerated” genes, but not “degenerated” genes. For both bulk- and single-cell analyses, gene expression and pathway enrichment analyses highlighted several pathways that may regulate CEP degeneration, including transcriptional regulation, translational regulation, intracellular transport, and mitochondrial dysfunction. Conclusions: This thorough analysis using RNA-Sequencing methods highlighted numerous differences between non-degenerated and degenerated CEP cells, the phenotypic heterogeneity of CEP cells, and several pathways of interest that may be relevant in CEP degeneration.
2024-01-10 | GSE242443 | GEO
Project description:To get insight into the genetic characteristics of hyper active mutant line of rat, SPORTS, and the effect of exercise on gene expression, we compared gene expression profiles of exercised SPORTS rat, sedentary SPORTS rat, and sedentary wild type rat. Using RNA extracted from the muscle of these rats, we performed microarray analysis. Subsequent GO analyses revealed that genes belonging to muscle development and glycolysis were upregulated in exercised SPORTS rat compared to sedentary SPORTS rat, and genes related to coagulation were upreguated in sedentary SPORTS rat compared to wild type rat. These results were consistent with phenotypes, such as hyper activity and thrombotic tendency, which were reported for SPORTS rat.
2018-11-01 | GSE88853 | GEO
Project description:A spontaneously phenotypically degenerated strain of M. robertsii strain ARSEF 2575 (M. robertsii lc2575; lc = low conidiation) showed a reduction in conidiation and fungal virulence after successive subculturing on artificial medium. However, the conidial production and fungal virulence of a phenotypically degenerated M. robertsii were recovered by serially passaging through a plant host. The DNA methylation level of phenotypically degenerated Metarhizium robertsii M. robertsii lc2575 and this fungi after solider bean passages were tested through the whole genome bisulfite sequencing. The results showed that approximately 0.379 % of cytosines are methylated in the fungi after bean passages, almost the same as the DNA methylation level in M. robertsii lc2575 (0.375%). The distribution of different methylated regions located more on intergenic regions of fungi after bean passages than M. robertsii lc2575. Gene Ontology (GO) analysis and KEGG analysis of DMR-associated genes revealed that amino acid, carbohydrate and fatty acid metabolism.
2020-03-03 | GSE146251 | GEO
Project description:Analysis of DOPA in the alpha 2 chain of type I collagen from rat tendon
2020-03-03 | MSV000085052 | MassIVE
Project description:We sought to confirm the genetic influence in the development of Ventilation-Associated Lung Injury (VALI) and, in the process, identify potential candidate genes involved in the disease by integrating differential gene expression profiling on rat lungs to a traditional strain survey analysis of the parental rat strains, VALI-sensitive Brown Norway rats versus VALI-resistant Dahl Salt Sensitive rats, comparing control (under room air ventilation) versus under high tidal volume (HTV) ventilation. We used microarrays to detail the global programme of gene expression underlying VALI susceptibility and identified distinct classes of up-regulated and down-regulated genes during this process. Keywords: strain-condition analysis
2007-02-15 | GSE7041 | GEO
Project description:To understand the impact of strain degeneration on the transcriptome we performed fermentations and RNA seq analysis to on a degenerated C.berijeirnckii strain.
2020-06-30 | E-MTAB-9201 | biostudies-arrayexpress
Project description:PurposeTo evaluate differences of Achilles tendon (AT) hardness and morphology between asymptomatic tendons in patients with acute AT ruptures on the contralateral side and asymptomatic tendons in healthy people by using computer-assisted quantification on axial-strain sonoelastography (ASE).MethodsThe study consisted of 33 asymptomatic tendons in 33 patients (study group) and 34 tendons in 19 healthy volunteers (control group). All the tendons were examined by both ASE and conventional ultrasound. Computer-assisted quantification on ASE was applied to extract hardness variables, including the mean (Hmean), 20th percentile (H20), median (H50) and skewness (Hsk) of the hardness within tendon, and the ratio of the mean hardness within tendon to that outside tendon (Hratio) and three morphological variables: the thickness (THK), cross-sectional area, and eccentricity (ECC) of tendons.ResultsThe Hmean, Hsk, H20, H50, and Hratio in the proximal third of the tendon body in study group were significantly smaller than those in control group (Hmean: 0.43±0.09 vs 0.50±0.07, p=0.001; Hsk: -0.53±0.51 vs -1.09±0.51, p<0.001; H20: 0.31±0.10 vs 0.40±0.10, p=0.001; H50: 0.45±0.10 vs 0.53±0.08, p<0.001; Hratio: 1.01±0.25 vs 1.20±0.23, p=0.003). The THK and cross-sectional area of tendons in the study group were larger than those in the control group (p<0.05).ConclusionsAs a quantitative objective method, the computer-assisted ASE reveals that the asymptomatic ATs contralateral to acute rupture are softer than those of healthy control group at the proximal third and the asymptomatic tendons in people with rupture history are thicker, larger, and rounder than those of normal volunteers especially at the middle and distal thirds of AT body.
| S-EPMC6304598 | biostudies-literature