Project description:The purpose of the present work was to examine gene expression patterns in a rat keratinocyte line exposed to a 56Fe ion beam Experiment Overall Design: The cells were exposed to 1.01 geV/nucleon 56Fe ions generated by the NASA Space Radiation Laboratory facility. Data from Affymetrix rat microarrays (RAT 230_2) were processed by BRB ArrayTools 3.3.0 software, and the Gene Ontogeny (GO) database was utilized to categorize significantly responding genes.
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).
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.
Project description:Little is known about molecular mechanism for its effectiveness of C-ions in melanomas. In this study, we examined the cytotoxic effects of C-ions on 6 human malignant melanoma cell lines, and gene expression profiles and cell cycle progression were also examined to reveal the mechanism of the therapeutic effectiveness of C-ions. Equivalent doses of the C-ions were more effective at reducing the survival rates than X-rays, and the relative biological effectiveness (RBE) was > 2.0 in all cell lines. In unsupervised 2D clustering performed for C-ions irradiated groups at 1 h after irradiation, many of the probes were down-regulated among 6 cell lines. We identified probes, such as XKRY, ELA3A, T-STAR, SCN9A, ELA2A, CRK7, CCNA2, CROP, CYR61, SDFR1, and SMAD4 differentially responded to C-ions and X-rays among 4 cell lines. CCNA2 was down-regulated by C-ions more than X-rays at 3 h after irradiation, and C-ions induced G2/M arrest more than X-rays in three cell lines at 30 h. Many of p53 target genes, such as ATF3, BTG2, CDKN1A, GADD45A, SESN1, and TNFRSF6 were up-regulated by C-ions at 3 h. The expressions of p53 target genes were not changed in HMV-I and MeWo. In MeWo, APG3L, RPL26 and PCNA were down-regulated or E2F2 and LIMS3 were up-regulated, and in HMV-I, ATF3, FOS, and CYR61 were up-regulated at 1 h after C-ions. In conclusion, C-ions affected p53-dependent and p53-independent pathways of cell death and cell cycle. Individual mechanism in activating of cell death was observed in each cell line of 6 melanomas. Keywords: Specific gene expression prfiles after carbon ion irradiation
Project description:The purpose of the present work was to examine gene expression patterns in a rat keratinocyte line exposed to a 56Fe ion beam Keywords: Dose response
Project description:In order to establish a rat embryonic stem cell transcriptome, mRNA from rESC cell line DAc8, the first male germline competent rat ESC line to be described and the first to be used to generate a knockout rat model was characterized using RNA sequencing (RNA-seq) analysis.