Expression data from kidney transplantations in a Fisher-Lewis rat model: placebo and 13cisRA treatment
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE17045 | GEO | 2012/01/07
SECONDARY ACCESSION(S): PRJNA117851
REPOSITORIES: GEO
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Project description:Most kidney allograft losses are caused by chronic allograft dysfunction (CAD). The aim of the study was to correlate changes in gene expression over time during the development of chronic damage in contrast to13cisRA Treated animal that demonstrated morphologically healthy kidneys by the end of teh study. Renal allografts were harvested from placebo and13cisRA Treatment groups for time points 0d, 7d, 14d and 56d (n=3-5) and examined for steady state mRNA expression using Affymetrix microarray RG-U34A. The effect of the13cisRA Treatment on dysregulated pathways was examined. In order to verify the microarray analysis, qPCR has been performed. Microarray data was used to obtain transcriptomic changes reflecting signaltransduction pathway dysregulation Progression of rejection was observed in untreated animals at timepoints 7d, 14d and 56d after transplantation that could be prevented by 13cisRA treatment
2012-01-07 | E-GEOD-17045 | biostudies-arrayexpress
Project description:Most kidney allograft losses are caused by chronic allograft dysfunction (CAD) that is characterized by interstitial fibrosis, tubular atrophy and a smoldering inflammatory process. The aim of the study was to correlate changes in gene expression over time, as evidenced by effects on regulatory pathways linked to the development of fibrosis and inflammation during the development of chronic damage. Renal allografts were harvested for time points 0d, 7d, 14d and 56d (n=3-5) and examined for steady state mRNA expression using Affymetrix microarray RG-U34A. A select group of genes previously associated with chronic fibrosis was then examined in the context of progressive dysfunction. In order to verify the microarray analysis, qPCR has been performed. Microarray data was used to obtain transcriptomic changes reflecting signaltransduction pathway dysregulation Timecourse results (log2 placebo/control) linked below as supplementary files. Keywords: timecourse analysis
2009-10-01 | GSE13368 | GEO
Project description:We used microarrays to distinguish the gene expression differences among different time points after injury. We generated L4-6 dorsal root ganglia (DRG) tissues and proximal sciatic nerve (SN) tissues (0.5cm) at 0d, 1d, 4d, 7d and 14d after sciatic nerve resection.
2013-01-01 | E-GEOD-30165 | biostudies-arrayexpress
Project description:Gene expression signatures following nerve injury in a rat model (0d-14d)
| PRJNA143815 | ENA
Project description:Altered microRNA expression in sciatic nerve following injury in rat model (0d-14d)
| PRJNA416322 | ENA
Project description:<br><br>Annual heart allograft failure in humans rates about 3-5%. The main reason after the first postoperative year is chronic rejection. Myointimal hyperplasia, the hellmark of chronic rejection, results in a specific type of ischemic heart disease. The lack of angina pectoris symptoms allow ventricular arrythmias, sudden cardiac death or heart failure to occur without warning. In addition, diagnostic tools such as endomyocardial biopsy, coronary angiography or intracoronary ultrasound fail to predict the individual risk for myocardial dysfunction.<br><br>The mechanisms responsible for chronic rejection are predominantly alloimmune mediated with activated T cells, macrophages, B cell mediated antibody formation and secreted cytokines responding to HLA and other endothelial cell antigens. In addition, non immunologic risk factors such as recipient age, metabolic factors, hypertension and ischemia contribute to development of this disease. Previous studies have demonstrated that ischemia has a profound influence on short term allograft survival but the underlaying mechanisms remain largely unknown. Apoptosis seems to play a crucial role in ischemia/reperfusion injury and several mechanisms for programmed cell death have been described. However, consequences on long term cell function of viability have not been investigated. <br><br>The aim of this study was to investigate the implication and the mechanism of prolonged cold organ storage as a non immunologic risk factor in the pathogenesis of chronic rejection in a cardiac allograft model. <br><br>We aimed for answering the following specific questions:<br><br>How does cold ischemia affect the alloimmue response short and long term? <br><br>How does prolonged cold ischemia affect gene expression at later time points after transplantation? <br><br>Does it influence gene expression during chronic rejection?<br><br><br><br>
2010-10-13 | E-MEXP-2301 | biostudies-arrayexpress
Project description:Advancements in animal models and cell culture techniques have been invaluable in the elucidation of molecular events and mechanisms regulating muscle atrophy. However, few studies have examined muscle atrophy in humans using modern experimental techniques. The purpose of this study was to examine and validate changes in global gene transcription during immobilization-induced muscle atrophy in humans. Healthy men and women (N=24) were subjected to two weeks of unilateral limb immobilization, with muscle biopsies obtained before, and after 48 hours (48H) and 14 days (14D) of immobilization. Both muscle cross sectional area (~ 5 %) and strength (10-20 %) were significantly reduced in men and women after 14D of immobilization. Micro-array analysis of total RNA extracted from biopsy samples uncovered 575 and 3,128 probes representing multiple genes, which were significantly altered at 48H and 14D, respectively. As a group, genes involved in mitochondrial bioenergetics and carbohydrate metabolism were predominant features at both 48H and 14D, with genes involved in protein synthesis and degradation significantly down-regulated and up-regulated, respectively, at 14D of muscle atrophy. There was also a significant decrease in the protein content of mitochondrial cytochrome c oxidase, and the enzyme activity of cytochrome c oxidase and citrate synthase after 14D of immobilization. Furthermore, protein ubiquitination and oxidative damage were significantly increased by 48H and 14D of immobilization, respectively. These results suggest that transcriptional and post-transcriptional suppression of mitochondrial processes is sustained throughout 14D of immobilization, while protein ubiquitination plays an early but transient role in the progression of immobilization-induced muscle atrophy in humans.
2009-02-21 | GSE14901 | GEO
Project description:OBJECTIVE: To study the genetic regulatory mechanisms in the remote zone of left ventricular (LV) free wall in order to partly explain the more frequent progression to heart failure after acute myocardial infarction (AMI) in diabetic rats. METHODS: 10 weeks after diabetes mellitus (DM) induction with Streptozotocin (STZ), the left anterior descending coronary arteries of uncontrolled diabetic Sprague-Dawley (SD) rats and non-diabetic ones were ligated without reperfusion. Then, the remote zone tissues of LV free wall were taken as samples at day 1, 7, 14, 28, and 56 post AMI. Significant different expression genes were filterd from Affymetrix Genechip U230 2.0 array by GCOS software. Genetic changes post myocardial infarction were classified by hierarchical clustering of 10 gene chips. And then, the differential expressions of 10 selected transcripts identified by the microarray were examined in greater detail by Real Time-PCR. RESULTS: According to hierarchical clustering, we find that the molecular regulatory expression related to cardiac remodeling in the remote zone to myocardial infarction is quite different as time elapses in both diabetic and non-diabetic rats. The gene expression at day 1 and 7 post AMI in both groups is similar, while the genetic changes at day 14 post AMI in diabetic rats and the ones at day 14 and 28 in non-diabetic rats are classified into the same cluster. And then the genetic changes at day 28 and 56 post AMI in diabetic rats and the ones at day 56 in non-diabetic rats are classified into the same cluster. (Figure.1) The patterns of numerous products of genes expression were used in the cluster, including 118 genes, such as leucine-rich PPR-motif containing (IL-6 signaling pathway), procollagen type I, VI, VIII, and XV, fibronectin1, RT1, and TIMP-1, etc. CONCLUSION: The genetic findings in this study might be the possible mechanism that diabetes mellitus can accerate the progression of post-infarction genetic regulatory expression. Experiment Overall Design: All studies were performed with male SD rats (200-220g), aged 8 weeks, which were obtained from laboratorial animal center of Chinese University of Agriculture. DM was induced with a singleintraperitoneal injection of STZ (65 mg/kg in 0.1mmol/L, pH 4.5 sodium citrate buffer) . Age and body weight matched rats that used as non-diabetic controls were injected with the same dose of sodium citrate buffer (0.1mmol/L, pH 4.5). Ultrastructure changes of myocardium were observed 10 weeks after DM induction by TEM. 10 weeks after DM induction,both diabetic and non-diabetic rats were subjected to left anterior descending coronary artery (LADCA) ischemia for 1-56 days without reperfusion. Two-dimensional echocardiography was utilized to obtain LV dimensions and LV percent fractional shortening at baseline, DM 10weeks, and at 1d, 7d, 14d, 28d, 56d after AMI; the remote zone tissues of LV free wall were taken as samples at day 1, 7, 14, 28, and 56 post AMI for gene chip microarray analysis (10 samples from 30 rats); in addition, heart-to-body weight and heart to tibial length ratios and masson's trichrome staining was measured as an index of cardiac hypertrophy and fibrosis at baseline, DM 10weeks, and at 1d, 7d, 14d, 28d, 56d after AMI.
2009-09-12 | E-GEOD-12639 | biostudies-arrayexpress
Project description:We have compared the gene expression profile of rat Achilles tendon-derived stem cells in post-natal tendon development. Rat tendon stem/progenitor cells (TSPCs) were isolated at different stages of post-natal development: TSPCs-1d, TSPCs-7d and TSPCs-56d. TSPCs at different post-natal development stages (1d, 7d and 56d) were isolated, cultured and used for microarray analyses at passage 2. All TSPCs in this study were of isolated from more than one individual. Total RNA was extracted and fragmented biotin-tagged cRNA was hybridized to Rat Genome 230 2.0 Array.
2015-07-10 | E-GEOD-68485 | biostudies-arrayexpress
Project description:Bud formation is an adaptive trait that temperate forest trees have acquired to facilitate seasonal synchronization. We have characterized transcriptome-level changes that occur during bud formation of white spruce (Picea glauca [Moench] Voss.), a primarily determinate species in which preformed stem units contained within the apical bud constitute most of next season's growth. Microarray analysis identified 4460 differentially expressed sequences in shoot tips during short day-induced bud formation. Cluster analysis revealed distinct temporal patterns of expression, and functional classification of genes in these clusters implied molecular processes that coincide with anatomical changes occurring in the developing bud. Comparing expression profiles in developing buds under long day and short day conditions identified possible photoperiod-responsive genes that may not be essential for bud development. Several genes putatively associated with hormone signalling were identified, and hormone quantification revealed distinct profiles for ABA, cytokinins, auxin and their metabolites that can be related to morphological changes to the bud. Comparison of gene expression profiles during bud formation in different tissues revealed 108 genes that are differentially expressed only in developing buds and show greater transcript abundance in developing buds than other tissues. These findings provide a temporal roadmap of bud formation in white spruce. Shoot tips (terminal buds), needles, and secondary stems were collected from two-year-old white spruce plants over a 10-week time course of 0, 1, 3, 7, 14, 28, and 70 days after switching from 6 to 8 weeks of long daylight photoperiods (LD; 16 hours of light and 8 hours of dark) to short daylight photoperiods (SD; 8 hours of daylight and 16 hours of dark). Remaining plants were kept in short days for an additional 8-15 weeks, and then transferred to low temperature (LT; 2°C to 4°C) for 3 to 4 weeks with continuing SD prior to harvest. Another set of plants was grown and harvested under the same conditions as described above, but remained in LD at all times. Four sets of dye-swap design microarray experiments were conducted. The first set of experiments (samples 1-7) studied the SD time course of buds development. Terminal buds from each time point (1d, 3d, 7d, 14d, 28d, and 70d) and LT were co-hybridized with actively growing shoot tips (0d). The same time point comparison (without LT) of shoot tips from LD-treated trees was carried out as the second set of experiments (samples 8-13). The third experiment (samples 14-20) denoted a separate LD/SD comparison at seven different time points (0d, 1d, 3d, 7d, 14d, 28d, and 70d), and the last experiment (samples 21-26) compared SD shoot tips, needles, and secondary stems with each of the other tissues at 14d and 70d. In each experiment, four biological replicates were used, with two replicates representing the dye-swaps.
2010-12-01 | E-GEOD-23519 | biostudies-arrayexpress