Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1063840 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27544949_1.fastq.gz | Fastqsanger.gz | |||
| SRR27544949_2.fastq.gz | Fastqsanger.gz | |||
| SRR27544950_1.fastq.gz | Fastqsanger.gz | |||
| SRR27544950_2.fastq.gz | Fastqsanger.gz | |||
| SRR27544951_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The objective of this study is to reveal the potential effects of CuO nanoparicles (NPs) on Desulfovibrio vulgaris Hildenborough (D. vulgaris) via genome-wide RNA sequencing Methods: RNA was harvested from D. vulgaris cultures in the presence and absence of CuO NPs (0, 1, 50, 250 mg CuO NPs/L) 8 h after cultivation.
2019-08-01 | GSE101911 | GEO
Project description:The C57BL/6J mice were randomly divided into three groups: control group (n=3), CuO NPs group (n=3), and CuO NPs + TTM group (n=3). A suspension of 2 mg/mL CuO NPs in 100 μl sterile saline was directly once administered by intratracheal instillation in CuO NPs treatment group. Mice in control group received 100 μl sterile saline. In the CuO NPs + TTM intervention group, 0.02 mg/mL TTM was added to the daily drinking water. All mice were sacrificed on day 7. Total RNA of the mouse lung tissues were extracted using tissue RNA isolation kit. All samples were sent to Majorbio Biotech (Shanghai, China) for transcriptome sequencing.
2025-01-13 | GSE286391 | GEO
Project description:This study proposes a molecular mechanism for lung epithelial A549 cell response to copper oxide nanoparticles (CuO-NPs) related to Cu ions released from CuO-NPs. Cells that survived exposure to CuO-NPs arrested the cell cycle as a result of the downregulation of proliferating cell nuclear antigen (PCNA), cell division control 2 (CDC2), cyclin B1 (CCNB1), target protein for Xklp2 (TPX2), and aurora kinase A (AURKA) and B (AURKB). Furthermore, cell death was avoided through the induced expression of nuclear receptors NR4A1 and NR4A3 and growth arrest and DNA damage-inducible 45 β and γ (GADD45B and GADD45G, respectively). The downregulation of CDC2, CCNB1, TPX2, AURKA, and AURKB, the expressions of which are involved in cell cycle arrest, was attributed to Cu ions released from CuO-NPs into medium. NR4A1 and NR4A3 expression was also induced by Cu ions released into the medium. The expression of GADD45B and GADD45G activated the p38 pathway that was involved in escape from cell death. The upregulation of GADD45B and GADD45G was not observed with Cu ions released into medium but was observed in cells exposed to CuO-NPs. However, because the expression of the genes was also induced by Cu ion concentrations higher than that released from CuO-NPs into the medium, the expression appeared to be triggered by Cu ions released from CuO-NPs taken up into cells. We infer that, for cells exposed to CuO-NPs, those able to make such a molecular response survived and those unable to do so eventually died. Two-condition experiment, CuO-NPs exposured vs. non-treated cells. Hybridization: 2 replicates. Scanning: 3 replicates (Gain changed).
2012-01-05 | E-GEOD-33278 | biostudies-arrayexpress
Project description:The in vitro and in vivo toxicity of copper oxide nanoparticles (CuO NPs) is attributed to both particle and dissolved copper ion species. However, a clear understanding of 1) the specific cellular responses that are modulated by the two species and 2) the temporal dynamics in toxicity, as the proportional amount of particulate and ionic forms change over time, is lacking. In the current study, in vitro responses to microparticulate CuO (CuO MPs), CuO NPs, and dissolved Cu2+ were characterized in order to elucidate particle and ion induced kinetic effects. Particle dissolution experiments were carried out in relevant cell culture medium, using CuO NPs and MPs. Mouse lung epithelial cells were exposed for 2 - 48 h with 1 - 25 µg/mL CuO MPs, CuO NPs, or 7 & 54 µg/mL CuCl2. Cellular viability and genome-wide transcriptional responses were assessed. Dose and time dependent cytotoxicity was observed in CuO NP exposed cells, which was delayed and subtle in CuCl2 and not observed in CuO MPs treated cells. Analyses of differentially expressed genes and associated pathway perturbations showed that dissolved ions released by CuO NPs in extracellular medium are insufficient to account for the observed potency and cytotoxicity. Further organization of gene expression results in an Adverse Outcome Pathway (AOP) framework revealed a series of key events potentially involved in CuO NPs toxicity. The AOP is applicable to soluble metal oxide nanoparticle induced toxicity in general, and thus, can facilitate the development of in vitro alternative strategies to screen their toxicity.
2022-11-03 | GSE161017 | GEO
Project description:This study proposes a molecular mechanism for lung epithelial A549 cell response to copper oxide nanoparticles (CuO-NPs) related to Cu ions released from CuO-NPs. Cells that survived exposure to CuO-NPs arrested the cell cycle as a result of the downregulation of proliferating cell nuclear antigen (PCNA), cell division control 2 (CDC2), cyclin B1 (CCNB1), target protein for Xklp2 (TPX2), and aurora kinase A (AURKA) and B (AURKB). Furthermore, cell death was avoided through the induced expression of nuclear receptors NR4A1 and NR4A3 and growth arrest and DNA damage-inducible 45 β and γ (GADD45B and GADD45G, respectively). The downregulation of CDC2, CCNB1, TPX2, AURKA, and AURKB, the expressions of which are involved in cell cycle arrest, was attributed to Cu ions released from CuO-NPs into medium. NR4A1 and NR4A3 expression was also induced by Cu ions released into the medium. The expression of GADD45B and GADD45G activated the p38 pathway that was involved in escape from cell death. The upregulation of GADD45B and GADD45G was not observed with Cu ions released into medium but was observed in cells exposed to CuO-NPs. However, because the expression of the genes was also induced by Cu ion concentrations higher than that released from CuO-NPs into the medium, the expression appeared to be triggered by Cu ions released from CuO-NPs taken up into cells. We infer that, for cells exposed to CuO-NPs, those able to make such a molecular response survived and those unable to do so eventually died.
2012-01-05 | GSE33278 | GEO
Project description:The three groups of MH-S cells were control group, 20 μg/ml CuO NPs group, and 20 μg/ml CuO NPs + 10 μM TTM group. Total RNA of the MH-S cells were extracted using cell RNA isolation kit (Vazyme Biotech Co., Ltd, China). The number of MH-S cell sample for each group were three (n = 3 cell samples/group). All samples were sent to Majorbio Biotech (Shanghai, China) for transcriptome sequencing.
2025-01-17 | GSE287049 | GEO
Project description:Nanomaterials (NMs) are on the nanoscale level range ca. 1-100 nm and due to the peculiar physico-chemical properties are widely used in different areas. The present study aimed to characterize the responses of zucchini (Cucurbita pepo L.) treated with copper oxide (CuO) NPs from seed germination to the flowering stage. CuO NPs treatment did not negatively impact plant morphology and growth as well as the pollen formation and viability. Physiological analyses were followed by a complete RNAseq-based transcriptomic analysis in the different plant tissues. Mitochondrial and chloroplast functions emerged as a critical component in plant response. Evidence of CuO NPs internalization and biotransformation was a driving force to measure the impacts at both physiological and molecular levels.
2021-07-25 | GSE173716 | GEO
Project description:This study investigated the pulmonary toxicity of Copper oxide nanoparticles (CuO NPs) surface modified with polyethylenimine (PEI) or ascorbate (ASC), was investigated. Rats were exposed nose-only to a fixed exposure concentration of ASC or PEI coated CuO NPs for 5 consecutive days. On day 6 and day 27 post-exposure, pulmonary toxicity markers in bronchoalveolar lavage fluid (BALF) were analyzed and histopathological evaluation of the lungs was performed, along with microarray analyses on whole lung tissue samples.
2020-10-02 | GSE158900 | GEO
Project description:The goals of this study are to use Next-generation sequencing (NGS) to detect bacterial mRNA profiles of E. coli K-12 LE392, P. putida KT2440 and IncPα RP4 plasmid, and their mRNA response under the exposure of CuO NPs and Cu2+. The concentrations were 5 μmol/L for CuO NPs and Cu2+. The group without dosing CuO NPs or Cu2+ was the control group. Each concentration was conducted in triplicate. By comparing the mRNA profiles of experimental groups and control group, the effects of these CuO NPs and Cu2+ on transcriptional levels can be revealed. Illumina HiSeq 2500 was applied. The NGS QC toolkit (version 2.3.3) was used to treat the raw sequence reads to trim the 3’-end residual adaptors and primers, and the ambiguous characters in the reads were removed. Then, the sequence reads consisting of at least 85% bases were progressively trimmed at the 3’-ends until a quality value ≥ 20 were kept. Downstream analyses were performed using the generated clean reads of no shorter than 75 bp. The clean reads of each sample were aligned to the E. coli reference genome (NC_000913), P.putida reference genome (NC_002947), and IncPα plasmid reference genome (NC_00) using SeqAlto (version 0.5). Cufflinks (version 2.2.1) was used to calculate the strand-specific coverage for each gene, and to analyze the differential expression in triplicate bacterial cell cultures. The statistical analyses and visualization were conducted using CummeRbund package in R (http://compbio.mit.edu/cummeRbund/). Gene expression was calculated as fragments per kilobase of a gene per million mapped reads (FPKM, a normalized value generated from the frequency of detection and the length of a given gene.
2022-05-15 | GSE131228 | GEO
Project description:Copper oxide nanoparticles (CuO NPs) are considered for various technological and consumer applications, leading to growing concerns for potential human hazards resulting from inhalation. Recent studies have revealed a dose-dependent toxicity of CuO NPs in rats following short-term inhalation exposure. Here, we utilized transcriptomics approaches to further investigate the responses in rats exposed via inhalation for five consecutive days to two doses of CuO NPs, 3.3 (low dose, LD) and 13.2 (high dose, HD) mg/m3, with collection of lung tissues on days 6 (1 day post-exposure) and 28 (i.e., after a 22-day post-exposure recovery period). Histopathology confirmed an acute inflammatory response that was resolved during the post-exposure phase. Global gene expression analyses yielded about 1,000 differentially expressed genes in HD rats and 200 in LD on day 6, and less than 20 after the recovery period. Pathway analysis indicated cell proliferation/survival and inflammation as the main processes triggered by exposure and identified epithelial cell transforming protein 2 (Ect2) as a potential gene of interest implicated in cell proliferation. Indeed, ECT2 was upregulated in exposed lungs and was localized in the cytoplasm of alveolar epithelial cells in HD rats, in hyperplasic foci identified based on the Ki67 antigen, a marker of cell proliferation. Monocyte chemoattractant protein 1 (MCP-1, also known as CCL2), with an important role in the regulation of inflammatory processes and cell proliferation, was also upregulated and this was confirmed immunohistochemically. Finally, we could not find any evidence for aberrant DNA methylation of inflammation-associated genes in response to CuO NP exposure. In summary, the current findings suggest that airborne CuO NPs cause an acute response that translates into inflammation and cellular proliferation in bronchoalveolar epithelium, with upregulation of neoplasia-related factors even after a short-term exposure.
2018-09-01 | GSE86390 | GEO