Time-Dependent miRNA Profiling Following Ischemia/Reperfusion Injury in Rat Retina
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE61072 | GEO | 2014/09/04
SECONDARY ACCESSION(S): PRJNA260187
REPOSITORIES: GEO
Similar Datasets
Project description:The purpose of the present study was to investigate time-dependent changes in the expression profile of miRNAs, following induction of IR in the rat retina, and to characterize the affected pathways, networks and processes. 6 biological replicates with two treatments (Sham control and Ischemia reperfusion) and 5 time points (0h, 2h, 24h, 48h and 7day) with total of 60 samples.
2014-09-04 | E-GEOD-61072 | biostudies-arrayexpress
Project description:The purpose of the present study was to investigate time-dependent changes in gene expression, following induction of IR in the rat retina, and to characterize the affected pathways, networks and processes.
2013-01-24 | GSE43671 | GEO
Project description:The purpose of the present study was to investigate time-dependent changes in gene expression, following induction of IR in the rat retina, and to characterize the affected pathways, networks and processes. 6 biological replicates with two treatments (Sham control and Ischemia reperfusion) and 3 time points (0h, 24h and 7day)
2013-01-24 | E-GEOD-43671 | biostudies-arrayexpress
Project description:Transcriptome profiling of the rat retina following ischemia-reperfusion injury
| PRJNA540770 | ENA
Project description:Transcriptomics has played valuable roles in deciphering differences between normal and diseased conditions at the molecular level. Herein is presented a transcriptome profile of ischemia-reperfusion (I/R) injury in adult Sprague-Dawley rat model and control group. Following acute I/R induction, a pool of the rats’ retinas at 12hr post I/R was made. RNA sequencing was performed on both the model and the control groups, followed by their transcriptomic analyses. Sample validation and quality control were done in accordance with standard protocols. Comparison of the sequenced data revealed significant variations in genes expression between the I/R model and their sham counterparts. These differentially expressed genes may provide valuable information to understanding the molecular mechanisms underlying retinal cell dysfunction, cell death and structure collapse in adult rats, and may help characterize or develop therapeutic interventions for visual impairment.
2022-05-01 | GSE130610 | GEO
Project description:This study was a part of a larger study assessing the response of young pigs to cardiac ischemia/reperfusion (IR) injury. A mild cardiac injury approach (IR) was used in post-weaned pigs (1-month), to assess regenerative repair in young large mammals after transient ischemic injury. Female and male postnatal day (P)30 pigs were subjected to cardiac ischemia (1-hour) by occlusion of the left anterior descending artery followed by reperfusion (IR), or to sham operation. In pigs subjected to IR, myocardial damage occurred, indicated by increased circulating cardiac troponin I 2-hours post-ischemia. In addition, cardiac ejection fraction (EF) was significantly decreased 2-hours post-ischemia and reduced EF was maintained to the 4-week study end-point. Histology demonstrated evidence of CM cell cycling at 2-months of age in multinucleated CMs in both sham-operated and IR pigs. Following IR, regional scar formation and inflammation in the epicardial region proximal to injury were observed 4-weeks post-IR. Sex differences in cardiac function and collagen deposition were found, highlighting the importance of representing both sexes in cardiac injury studies. Together, our results describe an effective novel cardiac injury model in 1-month old swine, at a time when CM are still cycling. However, pigs subjected to IR show a prolonged decrease in cardiac function, and the formation of a small, regional scar with increased inflammation. Together, these data demonstrate that 1-month old pigs do not regenerate myocardium, but form a scar, after transient IR injury.
2020-04-27 | GSE137293 | GEO
Project description:Ischemia-reperfusion (IR) injury, a ubiquitous consequence of liver transplantation, is a cause of early graft rejection and increased morbidity. At present, there are no effective strategies to reduce hepatic IR injury. Molecular mechanisms that promote cell survival under these circumstances are largely undefined. We examined changes in global gene expression at early reperfusion times to identify potential IR-mediated protective responses. Using a rat model of 30 minutes of 70% warm ischemia followed by reperfusion, RNA for microarray analysis was extracted from the non-ischemic and the ischemic-reperfused lobes at four reperfusion times: 0 (no reperfusion), 0.5, 2, and 6 hours. Differentially expressed genes and pathway analyses were used to identify IR-induced events. The transcriptome of the reperfused lobes was unique and discrete at each reperfusion time, showing no evidence of sustained changes of the gene expression alterations seen at 30 minutes of reperfusion. At all reperfusion times, a significant portion of gene expression changes in the reperfused lobes were present in the non-ischemic lobes. However, the earliest reperfusion time, 30 minutes, showed a marked increase in the expression of a set of immediate-early genes (c-Fos, c-Jun, Atf3, Egr1) that was exclusive to the reperfused lobe. Similarities of gene expression changes in the reperfused and the non-ischemic lobes at each time suggest that hemodynamics and/or circulating factors are potent stimuli in an IR model. However, early reperfusion events appear to reflect a cell-autonomous response that may be protective, thereby representing potential targets to ameliorate IR injury.
2019-12-16 | GSE117915 | GEO
Project description:Lung ischemia-reperfusion (IR) is known to occur after lung transplantation or cardiac bypass. IR leads to tissue inflammation and damage, is also associated with increased morbidity and mortality. Various receptors are known to partake in activation of innate immune system, but the downstream mechanism of tissue damage and inflammation is yet unknown. MicroRNAs (miRNA) are in the forefront in regulating ischemia reperfusion injury and are involved in inflammatory response. Here, we have identified by high throughput approach and evaluated distinct set of miRNAs that may play a role in response to IR in rat lung tissue. Top three differentially expressed miRNAs were validated through quantitative PCRs in the IR rat lung model and an in vitro model of IR of hypoxia and reoxygenation exposed type II alveolar cells. Among the miRNAs, miR-18a-5p showed consistent downregulation in both the model systems on IR. Cellular and molecular analysis brought to light a crucial role of this miRNA in ischemia reperfusion. MiR-18a-5p plays a role in IR mediated apoptosis, ROS production and regulates the expression of neuropeptide Galanin. It also influences the nuclear localization of transcription factor: Nuclear factor-erythroid 2 related factor (Nrf2) which in turn may regulate the expression of miR-18a gene. Thus, we have not only established a rat model for lung IR and enumerate the important miRNAs involved in IR but have also extensively characterized the role of miR-18a-5p in the same. This study will have important clinical and therapeutic implications for and during transplantation procedures.
2020-11-19 | GSE161520 | GEO
Project description:Lung ischemia–reperfusion (IR) injury increases the mortality and morbidity of patients undergoing lung transplantation. The objective of this study was to determine the key initiator of lung IR injury and to evaluate pharmacological therapeutic approaches using a functional inhibitor against the identified molecule. In a mouse hilar clamp model, the combination of RNA sequencing revealed that neutrophils-derived S100A8/A9 plays a central role in inflammatory reactions in lung IR injury.
2022-11-24 | GSE203238 | GEO
Project description:Sprague-Dawley rat retina post-injury and control samples Keywords = Gliosis, CNS injury
2004-03-29 | GSE1001 | GEO