Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA159147 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptomics Analysis of Lungs and Peripheral Blood of Crystalline Silica Exposed Rats
| PRJNA152883 | ENA
Project description:Living organisms are intricate systems with dynamic internal processes. Their RNA, protein, and metabolite levels fluctuate in response to variations in health and environmental conditions. Among these, RNA expression is particularly accessible for comprehensive analysis, thanks to the evolution of high throughput sequencing technologies in recent years. This progress has enabled researchers to identify unique RNA patterns associated with various diseases, as well as to develop predictive and prognostic biomarkers for therapy response. Such cross-sectional studies allow for the identification of differentially expressed genes (DEGs) between groups, but they have limitations. Specifically, they often fail to capture the temporal changes in gene expression following individual perturbations and may lead to significant false discoveries due to inherent noise in RNA sequencing sample preparation and data collection. To address these challenges, our study hypothesized that frequent, longitudinal RNA sequencing (RNAseq) analysis of blood samples could offer a more profound understanding of the temporal dynamics of gene expression in response to drug interventions, while also enhancing the accuracy of identifying genes influenced by these drugs. In this research, we conducted RNAseq on 829 blood samples collected from 84 Sprague-Dawley lab rats. Excluding the control group, each rat was administered one of four different compounds known for liver toxicity: tetracycline, isoniazid, valproate, and carbon tetrachloride. We developed specialized bioinformatics tools to pinpoint genes that exhibit temporal variation in response to these treatments.
2023-12-13 | GSE250058 | GEO
Project description:Expression data from rat peripheral blood mononuclear cells (PBMCs)
| PRJNA336375 | ENA
Project description:Diet induced gene expression in rat peripheral blood mononuclear cells
| PRJNA112525 | ENA
Project description:Improvements in the diagnosis and treatment of cancer has revealed the long-term side effects of chemotherapeutics, particularly cardiotoxicity. Current clinical measures to track cardiotoxicity are insufficient to diagnose damage before it has been done, necessitating new, early biomarkers of cardiotoxicity. Here, we collected paired transcriptomics and metabolomics data characterizing in vitro cardiotoxicity to three compounds: 5-fluorouracil, acetaminophen, and doxorubicin. Standard gene enrichment and metabolomics approaches identify some commonly affected pathways and metabolites but are not able to readily identify mechanisms of cardiotoxicity. Here, we integrate this paired data with a genome-scale metabolic network reconstruction (GENRE) of the heart to identify shifted metabolic functions, unique metabolic reactions, and changes in flux in metabolic reactions in response to these compounds. Using this approach, we are able to confirm known mechanisms of doxorubicin-induced cardiotoxicity and provide hypotheses for mechanisms of cardiotoxicity for 5-fluorouracil and acetaminophen.
2021-06-01 | GSE166957 | GEO
Project description:Enhancer Analysis in Peripheral Nerve Injury
| PRJNA266627 | ENA
Project description:Doxorubicin is a wildly used effective anticancer agent. However, doxorubicin use is also related to cardiotoxic side effect in some patients. Mitochondrial damage has been shown to be one of the pathogeneses of doxorubicin-induced myocardial injury. In this study, we test the hypothesis that mitochondrial transplantation might be a therapeutic strategy to prevent and ameliorate doxorubicin-induced cardiotoxicity. We demonstrated the deleterious effects of doxorubicin on mitochondrial structure and function in cardiomyocytes both in vitro and in vivo. Mitochondrial transplantation could inhibit doxorubicin-induced cardiotoxicity by directly supplying functional mitochondria. In vitro, mitochondrial transplantation improved contractile function and respiratory capacity, reduced cellular apoptosis and oxidative stress in cardiomyocytes. Mitochondria isolated from various sources, including mouse hearts, mouse and human arterial blood, and human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), all exerted similar cardioprotective effects. Mechanically, mitochondrial transplantation activates glutamine metabolism in doxorubicin-treated cardiomyocytes and blocking glutamine metabolism attenuated the cardioprotective effects of mitochondrial transplantation. Overall, our study demonstrates that mitochondria isolated from arterial blood could be used for mitochondrial transplantation, which might serve as a feasible promising therapeutic option for patients with doxorubicin-induced cardiotoxicity.
2025-03-13 | MTBLS7989 | MetaboLights
Project description:The FDA approved drug Doxorubicin provokes copious irreversible cardiotoxicity and even increases the risk of heart failure. Considering the multiple and interacted molecular pathways in cancer, there is a big possibility that tumors are simultaneously sensitive to different drugs. This makes achievable to study the combinations of drug, having the virtues of less toxicity, higher efficacy and potentially antagonizing drug resistance in cancer therapy. In the present study, we addressed the synergistic effects of ginsenoside Rh2 on doxorubicin-treated breast cancer bearing mice. We showed that Rh2 significantly enhanced the antitumor effects of doxorubicin and greatly attenuated the cardiotoxicity. Transcriptomic changes can clearly distinguish the chemotherapeutic groups and non-treated control groups. Transcriptomic analysis domestrated that Rh2 protection involved in multiple vital pathways including cellular senescece, fibrosis remodeling, apoptosis and inflammation.
2021-10-30 | GSE186765 | GEO
Project description:The FDA approved drug Doxorubicin provokes copious irreversible cardiotoxicity and even increases the risk of heart failure. Considering the multiple and interacted molecular pathways in cancer, there is a big possibility that tumors are simultaneously sensitive to different drugs. This makes achievable to study the combinations of drug, having the virtues of less toxicity, higher efficacy and potentially antagonizing drug resistance in cancer therapy. In the present study, we addressed the synergistic effects of ginsenoside Rh2 on doxorubicin-treated breast cancer bearing mice. We showed that Rh2 significantly enhanced the anti-cancer effects of doxorubicin and greatly attenuated the cardiotoxicity. Transcriptomic changes can clearly distinguish the chemotherapeutic groups and non-treated control groups. Transcriptomic analysis domestrated that Rh2 protection involved in multiple vital pathways including cellular stress, apoptosis and inflammation.
2021-10-28 | GSE186555 | GEO