Transcriptome profiling of cardiomyocytes treated with antioxidants
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PROVIDER: PRJNA839404 | ENA |
REPOSITORIES: ENA
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Project description:Despite clinical advancement, ischemia-induced myocardial diseases remain an underlying cause of death among individuals throughout the world. Interestingly, we found that the administration of antioxidants can protect cardiomyocytes during ischemia. However, the mechanism involved in inducing the cytoprotective effect under ischemic conditions is not fully elucidated. In this study, we carried out RNA-sequencing data analysis of rat ventricular cardiomyocytes under normoxic, ischemic, and ischemia with eugenol. The RNA sequencing data ascertained that the ischemic condition differentially regulated 7,694 genes in the NRVCs compared to the normoxic condition (padj<0.05). Out of 7,694 genes, 3,774 genes were up-regulated, and 3,920 genes were down-regulated. Also, the administration of eugenol in the presence of ischemic condition up-regulated 159 genes and down-regulated 111 genes. Functional enrichment analysis of differentially regulated genes was carried out using clusterProfiler R and ingenuity pathway analysis. In this study, we found that both the up-regulated and down-regulated genes regulated the post-translational modification of histone proteins during ischemia. Also, the up-regulated genes controlled cell death and survival, protein synthesis and transport etc. The down-regulated genes controlled cellular growth and development, cell signaling, cellular assembly and organization, cellular movement, cellular respiration, and cell death and survival. It was found that eugenol administration under ischemic conditions up-regulated intracellular transduction signaling and down-regulated negative regulation of the metabolic process, negative regulation of nucleic acid templated transcription, and negative regulation of the biosynthetic process. All in all, the administration of antioxidants improves cell survival via down-regulating negative regulation of biosynthetic processes.
2023-04-12 | GSE203313 | GEO
Project description:Transcriptome profiling of cardiomyocytes treated with antiretroviral drugs
| PRJNA777924 | ENA
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:Antioxidants are widely used to protect cells from damage induced by reactive oxygen species (ROS). The concept that antioxidants can help fight cancer is deeply rooted in the general population, promoted by the food supplement industry, and supported by some scientific studies. However, clinical trials have reported inconsistent results. Here, we show that supplementing the diet with the antioxidants N-acetylcysteine (NAC) and vitamin E markedly increases tumor progression and reduces survival in mouse models of B-RAF- and K-RAS-induced lung cancer. RNA sequencing revealed that NAC and vitamin E, which are structurally unrelated, produce highly coordinated changes in tumor transcriptome profiles, dominated by reduced expression of endogenous antioxidant genes. NAC and vitamin E increase tumor cell proliferation by reducing ROS, DNA damage, and p53 expression in mouse and human lung tumor cells. Inactivation of p53 increases tumor growth to a similar degree as antioxidants and abolishes the antioxidant effect. Thus, antioxidants accelerate tumor growth by inactivating the ROS-p53 axis. Because p53 inactivation occurs late in tumor progression, antioxidants may accelerate the growth of early tumors or precancerous lesions in high-risk populations such as smokers and patients with chronic obstructive pulmonary disease who receive NAC to relieve mucus production. There were 3 experimental groups (untreated, NAC-treated and Vitamin E-treated. Each group consisted of 5 animals, and from each animal we harvested 2 tumor samples. Hence, in total 3x10=30 samples were profiled.
2014-01-31 | E-GEOD-52594 | biostudies-arrayexpress
Project description:Antioxidants are widely used to protect cells from damage induced by reactive oxygen species (ROS). The concept that antioxidants can help fight cancer is deeply rooted in the general population, promoted by the food supplement industry, and supported by some scientific studies. However, clinical trials have reported inconsistent results. Here, we show that supplementing the diet with the antioxidants N-acetylcysteine (NAC) and vitamin E markedly increases tumor progression and reduces survival in mouse models of B-RAF- and K-RAS-induced lung cancer. RNA sequencing revealed that NAC and vitamin E, which are structurally unrelated, produce highly coordinated changes in tumor transcriptome profiles, dominated by reduced expression of endogenous antioxidant genes. NAC and vitamin E increase tumor cell proliferation by reducing ROS, DNA damage, and p53 expression in mouse and human lung tumor cells. Inactivation of p53 increases tumor growth to a similar degree as antioxidants and abolishes the antioxidant effect. Thus, antioxidants accelerate tumor growth by inactivating the ROS-p53 axis. Because p53 inactivation occurs late in tumor progression, antioxidants may accelerate the growth of early tumors or precancerous lesions in high-risk populations such as smokers and patients with chronic obstructive pulmonary disease who receive NAC to relieve mucus production.
2014-01-31 | GSE52594 | GEO
Project description:Background and Aims: It is known that inflammatory processes are activated in heart failure, but the regulation of cytokines and their role in the pathogenesis of the disease are not well understood. We have identified fractalkine as a possible novel mediator in HF development. To address this issue, we have performed microarray analysis of cardiomyocytes treated with different isoforms of fractalkine. Methods: Cardiomyocytes isolated from adult rat hearts and treated with different forms of fractalkine for 24 hours. Control cells were treated with BSA. Molecular alterations in myocardial tissue were measured by using cDNA microarrays. Molecular pathways affected were identified by the Ingenuity Pathway Analysis software. Results: Several molecular pathways were affected upon fractalkine stimulation of adult cardiomyocytes. Keywords: Fractalkines effect on cardiomyocytes
2008-02-01 | GSE7397 | GEO
Project description:Background and Aims: It is known that inflammatory processes are activated in heart failure, but the regulation of cytokines and their role in the pathogenesis of the disease are not well understood. We have identified fractalkine as a possible novel mediator in HF development. To address this issue, we have performed microarray analysis of cardiomyocytes treated with different isoforms of fractalkine. Methods: Cardiomyocytes isolated from adult rat hearts and treated with different forms of fractalkine for 24 hours. Control cells were treated with BSA. Molecular alterations in myocardial tissue were measured by using cDNA microarrays. Molecular pathways affected were identified by the Ingenuity Pathway Analysis software. Results: Several molecular pathways were affected upon fractalkine stimulation of adult cardiomyocytes. Experiment Overall Design: Cardiomyocytes isolated from adult rat hearts at three different timepoints. Five fractalkine treated samples and five control samples were pairwise analyzed. The cells were from three different isolations. Treated and untreated cells from the same isolation were compared on each microarray.
2008-06-18 | E-GEOD-7397 | biostudies-arrayexpress
Project description:RNA expression profiling in cardiomyocytes
| PRJNA420714 | ENA
Project description:Expression data from differently treated mouse cardiomyocytes
| PRJNA419008 | ENA
Project description:We wanted to analyze the global gene expression to unravel molecular mechanisms underlying the combined action of DOX and IFNγ in mouse cardiomyocytes. We treated the cardiomyocytes respectively with PBS, DOX and DOX plus IFN-γ, and the differentially expressed genes and the gene expression patterns were supposed to be analyzed.
2020-11-17 | GSE107113 | GEO