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Copper oxide nanoparticles treated MH-S cells

ABSTRACT: Copper oxide nanoparticles treated MH-S cells

PROVIDER: PRJNA1211049 | ENA |

REPOSITORIES: ENA

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Copper oxide nanoparticles treated C57 mice

Project description:Copper oxide nanoparticles treated C57 mice

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Copper oxide nanoparticles treated MH-S cells

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.

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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.

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Project description:Due to the wide application of rare earth oxides nanoparticles in different fields, they will inevitably be released into the environment, and their potential toxicity and ecological risks in the environment have become a concern of people. Yttrium oxide nanoparticles are important members of rare earth oxides nanoparticles. The molecular mechanism of its influence on plant growth and development and plant response to them is unclear. In this study, we found that yttrium oxide nanoparticles above 2 mM significantly inhibited the growth of Arabidopsis seedlings. Using the Arabidopsis marker lines reflecting auxin signal, it was found that the treatment of yttrium oxide nanoparticles led to the disorder of auxin signal in root cells: the auxin signal in quiescent center cells and columella stem cells decreased; while the auxin signal in the stele cells was enhanced. In addition, trypan blue staining showed that yttrium oxide nanoparticles caused the death of root cells. Transcriptome sequencing analysis showed that yttrium oxide nanoparticles specifically inhibited the expression of lignin synthesis related genes, activated mitogen-activated protein kinase (MAPK) signaling pathway, and enhanced ethylene and ABA signaling pathways in plants. This study revealed the phytotoxicity of yttrium oxide nanoparticles at the molecular level, and provided a new perspective at the molecular level for plants to respond to rare earth oxide stress.

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Transcriptomic profiling reveals differential cellular response of copper oxide nanoparticles and polystyrene nanoplastics in perfused human placenta

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Zinc oxide Nanoparticles exposure impairs cranial neural crest development by inducing oxidant stress during chicken embryogenesis

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Molecular responses of human lung epithelial cells to the toxicity of copper oxide nanoparticles inferred from whole genome expression analysis.

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 Î² and Î³ (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