RNA-seq of a high glucose induced oxidative stress and apoptosis model on primary rat cardiomyocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA430889 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Diabetic hyperglycemia promotes reactive oxygen species (ROS) production to lead to oxidative stress and apoptosis responsible for progressive deterioration of the structure and function of organs. It has been indicated that factors and pathways regulating ROS production and the cellular redox state play a key role in the progression of diabetes and diabetes complications including cardiomyopathy. Recent studies had demonstrated that long non-coding RNAs (lncRNAs) played crucial roles on modulation of oxidative stress and apoptosis activity. In this study, we first established a high glucose induced oxidative stress and apoptosis model on primary rat cardiomyocytes. ROS formation and apoptosis activity were significantly increased at 24h/48h after high glucose stimulation. RNA sequencing analysis was applied to detect differentially expressed lncRNAs during cardiomyocytes oxidative stress and apoptosis.
2019-01-19 | GSE109441 | GEO
Project description:Impact of glucose metabolism in postnatal cardiomyocytes
| PRJNA612444 | ENA
Project description:Analysis of human iPS-derived cardiomyocytes exposed to glucose, endothelin-1 and cortisol in vitro. Treatment produces a surrogate diabetic cardiomyopathic phenotype. Results provide insight into the pathways regulated by the treatment in the cardiomyocyte. The RNA for each vehicle-control treated and glucose endothelin cortisol treated iPS derived cardiomyocytes from 4 replicate samples, were extracted and hybridized to 8 individual human HG-U133 Plus2.0 Affymetrix microarray gene chips, whereby each chip represented the expression profile for one cell culture at 2 days.
2014-10-10 | E-GEOD-62203 | biostudies-arrayexpress
Project description:Apoptosis of vascular smooth muscle cells (VSMCs) is closely related to the pathogenesis of cardiovascular disease, and oxidative stress is an important cause for VSMCs death. Inhibiting VSMCs apoptosis is an effective preventive strategy in slowing down the development of cardiovascular disease, especially for atherosclerosis. In this study, we found OXR1 (oxidation resistance protein 1), a crucial participator for responding for oxidative stress, could modulate the expression of p53, a key regulator of apoptosis. Our results revealed that oxidative stress promoted VSMCs apoptosis by overexpression of OXR1-p53 axis, and 6-shogaol (6S), a major biologically active compound present in ginger, could effectively attenuate cell death by preventing the up-regulated expression of OXR1-p53 axis. Quantitative proteomics analysis revealed that the degradation of p53 mediated by OXR1 might related with the enhanced assembly of SCF ubiquitin ligase complexes, which is reported to closely relate with the modification of ubiquitination or neddylation, and subsequent degradation of p53.
2022-02-22 | PXD015127 | Pride
Project description:Glucose-lowering drugs sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of serious heart failure events, regardless of diabetes status, but the underling mechanism of this cardioprotective benefit is unknown. Here, we performed RNA-seq screening in cardiomyocytes to determine the potential cardioprotective mechanism of empagliflozin (EMPA).
2022-12-12 | GSE200598 | GEO
Project description:Analysis of human iPS-derived cardiomyocytes exposed to glucose, endothelin-1 and cortisol in vitro. Treatment produces a surrogate diabetic cardiomyopathic phenotype. Results provide insight into the pathways regulated by the treatment in the cardiomyocyte.
2014-10-10 | GSE62203 | GEO
Project description:Accumulating evidence suggests that new cardiomyocytes are generated from existing cardiomyocytes at a low rate throughout life. This limited regenerative capacity is unable to restore cardiac function after substantial cardiac damage; thus, small molecules have been examined for their ability to enhance the replication of existing cardiomyocytes. A novel compound TAZ-K promoted cardiomyocyte proliferation, therefore, we analyzed the effect of TAZ-K on gene expression in neonatal rat cardiomyocytes. Gene expression involved in cell cycle, anti-oxidant and anti-apoptosis was up-regulated. Thus, TAZ-K may have multifaceted effects and provide a treatment strategy that complements current therapies for patients with myocardial infarction.
2018-10-31 | GSE95274 | GEO
Project description: Not available
| S-EPMC3416810 | biostudies-literature
Project description:Pathogens have to cope with oxidative, iron- and carbon-limitation stresses in the human body. To understand how combined iron-carbon limitation alters oxidative stress response, Aspergillus fumigatus was cultured in glucose-peptone or peptone containing media supplemented or not with deferiprone as iron chelator. Changes in the transcriptome in these cultures were recorded after H2O2 treatment. Responses to oxidative stress were highly dependent on the availability of glucose and iron. Out of the 16 stress responsive antioxidative enzyme genes only the cat2 catalase-peroxidase gene was upregulated in more than two culturing conditions. The transcriptional responses observed in iron metabolism also varied substantially in these cultures. Only extracellular siderophore production appeared important regardless to culturing conditions in oxidative stress protection, while enhanced synthesis of Fe-S cluster proteins seemed to be crucial for oxidative stress treated iron-limited and fast growing (glucose rich) cultures. Although pathogens and host cells live together in the same place, their culturing conditions (e.g. iron availability, or occurrence of oxidative stress) can be different. Therefore, inhibition of a universally important biochemical process, like Fe-S cluster assembly, may selectively inhibit the pathogen growth in vivo and represent a potential target for antifungal therapy.
2024-04-03 | GSE256524 | GEO
Project description:Recent evidence suggests that hypoxia caused by acute myocardial infarction (AMI) can induce evident cardiomyocyte apoptosis. Exosomes, as paracrine signaling mediators by delivering cytosolic components (including miRNA, mRNA, protein), play crucial roles in intercellular communication. However, the systemic regulation of exosome-mediated miRNA delivery and subsequent regulation effect underlying AMI are not well-understood to date. Here, using small RNA-seq, we investigated the miRNAome of H9C2 cells and corresponding paracrine exosmes after hypoxia stress, and identified total of 92 and 62 differentially expressed (DE) miRNAs in cells and exosomes from hypoxia vs. normoxia condition. We found that hypoxia strongly induced the expression of hypoxamiRs in H9C2 cells and altered cardiomyocyte-derived exosomal miRNAome. Functional enrichment analysis revealed extensive roles of DE exosomal miRNAs in HIF-1 signaling pathway and cell apoptosis process, such as TNF signaling pathway, MAPK signaling pathway, mTOR signaling pathway. Furthermore, the gain- and loss-of-function analysis demonstrated the anti-apoptotic effects of hypoxia-induced exosomal miRNAs, i.e. miR-21-5p, miR-378-3p, miR-152-3p, let-7i-5p, and then the luciferase reporter assay confirmed that miR-152-3p and let-7i-5p implemented their anti-apoptotic function by directly targeting Atg12 and Faslg, respectively. In short, this study revealed that hypoxia-exosomes derived from cardiomyocyte, loaded abundant cardio-protective miRNAs, mediate crosstalk among cardiomyocytes and prevent cardiomyocytes apoptosis after hypoxia. Methods: we established the anoxia model using H9C2 cells, an immortal cardiac muscle cell line, to imitate hypoxia condition caused by AMI in vitro, and then small RNA-seq were employed to investigate the miRNA transcriptome of H9C2 cells and its exosomes collected from hypoxia and normoxia culture medium. Results: we identified the miRNAome of H9C2 cells and its exosmes under both hypoxia and normoxia, including 331, 338, 144, 74 unique mature miRNAs from hypoxia-cells, normoxia-cells, hypoxia-exosomes, normoxia-exosomes, respectively. Total of 92 and 62 DE miRNAs were identified from cells and exosomes. Among of which, the DE exosomal miRNAs were mainly involved in HIF-1 signaling pathway and cell apoptosis process, such as TNF signaling pathway, MAPK signaling pathway, mTOR signaling pathway. Interestingly, we found that some DE exosomal miRNAs, including miR-21-5p, miR-378-3p, miR-152-3p, let-7i-5p, have an anti-apoptotic and pro-viability effects in H9C2 cells under hypoxic stress. In addition, Atg12 and Faslg to be respective target of miR-152-3p and let-7i-5p were partly elucidated the anti-apoptosis mechanism of hypoxia-exosomes. Conclusions:In brief, this study illustrated a potential mechanism that, under hypoxic stress, hypoxia pre-perceived cardiomyocytes can spontaneously secrete the hypoxamiRs enriched exosomes, loaded a large amount of cardio-protective miRNA, which mediate crosstalk among cardiomyocytes and prevent apoptosis to heighten the hypoxia adaptability of cardiomyocytes. In more detail, we first discovered that miR-152-3p and let-7i-5p, enriched in hypoxia-exosomes derived by cardiomyocytes, played an anti-apoptosis role via mitochondrial pathway(intrinsic pathway) and death receptor pathway (extrinsic pathway), respectively.
2017-06-14 | GSE90123 | GEO