Rat cardiomyocyte: control vs diclofenac treatment
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE77880 | GEO | 2016/02/13
SECONDARY ACCESSION(S): PRJNA311943
REPOSITORIES: GEO
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Project description:Gene expression analysis of diclofenac-treated rat cardiomyocytes vs non-treated rat cardiomyocytes. Goal of study is to identify changes on genes expression induced by diclofenac. The data analysis focused on genes that might be related to cardiotoxicity; genes expression ion channels and pathways. two control samples vs 6 diclofenac-treated samples. Variables of treatment included two time points (6h or 24h) and three reference concentrations (1, 1/5 and 1/25). Each group had 3 replicates.
2016-02-13 | E-GEOD-77880 | biostudies-arrayexpress
Project description:Gene expression analysis of celecoxib-treated rat cardiomyocytes vs non-treated rat cardiomyocytes. Goal of study is to identify changes on genes expression induced by celecoxib. The data analysis focused on genes that might be related to cardiotoxicity; genes expression ion channels and pathways.
2016-02-05 | GSE77591 | GEO
Project description:Gene expression analysis of celecoxib-treated rat cardiomyocytes vs non-treated rat cardiomyocytes. Goal of study is to identify changes on genes expression induced by celecoxib. The data analysis focused on genes that might be related to cardiotoxicity; genes expression ion channels and pathways. two control samples vs 6 celecoxib-treated samples. Variables of treatment included two time points (6h or 24h) and three reference concentrations (1, 1/5 and 1/25). Each group had 3 replicates.
2016-02-05 | E-GEOD-77591 | biostudies-arrayexpress
Project description:Diclofenac is a widely used analgesic drug that can cause serious adverse drug reactions. We used Saccharomyces cerevisiae as model eukaryote to elucidate the molecular mechanisms of diclofenac toxicity and resistance. Although most yeast cells died during initial diclofenac treatment, some survived and started growing again. Microarray analysis of the adapted cells identified three major processes involved in diclofenac detoxification and tolerance. Especially pleiotropic drug resistance genes and genes under control of Rlm1p, a transcription factor in the protein kinase C (PKC) pathway, were upregulated in diclofenac-adapted cells. Genes involved in ribosome biogenesis and rRNA processing were downregulated, as well as zinc-responsive genes.
2011-05-17 | GSE29331 | GEO
Project description:Diclofenac is a widely used analgesic drug that can cause serious adverse drug reactions. We used Saccharomyces cerevisiae as model eukaryote to elucidate the molecular mechanisms of diclofenac toxicity and resistance. Although most yeast cells died during initial diclofenac treatment, some survived and started growing again. Microarray analysis of the adapted cells identified three major processes involved in diclofenac detoxification and tolerance. Especially pleiotropic drug resistance genes and genes under control of Rlm1p, a transcription factor in the protein kinase C (PKC) pathway, were upregulated in diclofenac-adapted cells. Genes involved in ribosome biogenesis and rRNA processing were downregulated, as well as zinc-responsive genes. Five independent yeast cultures were incubated with 100 µM diclofenac for 75 hours. Every 24h, cultures were diluted to OD600 ~0.1 in YNB containing 100 µM diclofenac. Five independent control cultures were grown in the absence of diclofenac.
2011-05-17 | E-GEOD-29331 | biostudies-arrayexpress
Project description:Diclofenac is widely used as nonsteroidal anti-inflammatory drug leaving residues in the environment. To investigate effects on terrestrial ecosystems, we measured dissipation rate in soil and investigated ecotoxicological and transcriptome-wide responses in Folsomia candida. Exposure for 4 weeks to diclofenac reduced both survival and reproduction of F. candida in a dose-dependent manner. At concentrations ≥200 mg/kg soil diclofenac remained stable in the soil during a 21-day incubation period. Microarrays examined transcriptional changes at low and high diclofenac exposure concentrations. The results indicated that development and growth were severely hampered and immunity-related genes, mainly directed against bacteria and fungi, were significantly up-regulated. Furthermore, neural metabolic processes were significantly affected only at the high concentration. We conclude that diclofenac is toxic to non-target soil invertebrates, although its mode of action is different from the mammalian toxicity. The genetic markers proposed in this study may be promising early markers for diclofenac ecotoxicity.
2014-10-01 | GSE59589 | GEO
Project description:The use of antiretroviral therapy (ART) improved the life expectancy of HIV patients through the suppression of HIV propagation in host. However, recent studies suggest that long-term use of ART induces comorbid conditions and heart failure in surviving HIV patients. The mechanism associated with the antiretroviral drugs (ARVs) induced cardiotoxicity and heart failure is not clear. In this study, we performed an RNA sequencing with ARV drugs-treated neonatal rat ventricular cardiomyocytes to explore drugs-induced cardiotoxicity. RNA-sequencing data analysis identified 1756 differentially expressed genes (padj<0.05) in cardiomyocytes. Out of 1756 genes, 701 genes were upregulated, and 1055 genes were downregulated in drug-treated cardiomyocytes. Functional enrichment analysis of differentially expressed genes was performed using clusterProfiler R and ingenuity pathway analysis. Our study showed that upregulated genes were linked with the biological processes associated with apoptosis, cellular movement or locomotion, cellular stress, and immune response. In contrast, down-regulated genes were involved in cell division and metabolism. Interestingly, we also found that ARV drugs treatment significantly upregulates the expression of a set of genes involved in cardiac enlargement and hypertrophy in the heart. Collectively, ARVs treatment in cardiomyocytes induces cardiotoxicity through differentially regulation of pathological genes expression in cardiomyocytes.
2021-12-29 | GSE188210 | GEO
Project description:Anthracyclines such as doxorubicin (Dox) are effective chemotherapeutic agents, however their use is hampered by subsequent cardiotoxicity risk. Our understanding of cardiomyocyte protective pathways activated following anthracycline-induced cardiotoxicity (AIC) remains incomplete. Insulin-like growth factor binding protein (IGFBP) 3 (Igfbp-3), the most abundant IGFBP family member in the circulation, is associated with effects on the metabolism, proliferation, and survival of various cells. Whereas Igfbp-3 is induced by Dox in the heart, its role in AIC is ill-defined. We investigated molecular mechanisms as well as systems-level transcriptomic consequences of manipulating Igfbp-3 in AIC using neonatal rat ventricular myocytes and human induced pluripotent stem cell-derived cardiomyocytes.
2022-06-28 | GSE206803 | GEO
Project description:Ketoprofen and diclofenac are non-steroidal anti-inflammatory drugs (NSAIDs) often used for similar indications, and both are frequently found in surface waters. Diclofenac affects organ histology and gene expression in fish at around 1 µg/L. Here, we exposed rainbow trout to ketoprofen (1, 10 and 100 µg/L) to investigate if this alternative causes less risk for pharmacological responses in fish. The bioconcentration factor from water to fish blood plasma was <0.05 (4 for diclofenac based on previous studies). Ketoprofen only reached up to 0.6‰ of the human therapeutic plasma concentration, thus the probability of target-related effects was estimated to be fairly low. Accordingly, a comprehensive analysis of hepatic gene expression revealed no consistent responses. In some contrast, trout exposed to undiluted, treated sewage effluents bioconcentrated ketoprofen and other NSAIDs much more efficiently, according to a meta-analysis of recent studies. Neither of the setups is however an ideal representation of the field situation. If a controlled exposure system with a single chemical in pure water is a reasonable representation of the environment, then the use of ketoprofen is likely to pose a lower risk for wild fish than diclofenac, but if bioconcentration factors from effluent-exposed fish are applied, the risks may be more similar.
2012-06-01 | GSE37628 | GEO
Project description:We performed RNA-Seq analysis of neoatal rat ventricular cardiomyocytes (NRVCs) and human pluripotent stem cells derived cardiomyocytes (hPSC-CMs) which were treated with Nimodipine (NM) to investigate the moleclular mechanism of inhibiting L-type calcium channel (LTCC) to promote cardiomyocyte proliferation.
2022-10-10 | GSE185542 | GEO