Ontology highlight
ABSTRACT:
PROVIDER: PRJNA893197 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR22046638_1.fastq.gz | Fastqsanger.gz | |||
| SRR22046638_2.fastq.gz | Fastqsanger.gz | |||
| SRR22046639_1.fastq.gz | Fastqsanger.gz | |||
| SRR22046639_2.fastq.gz | Fastqsanger.gz |
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Project description:The rainbow trout, Oncorhynchus mykiss, is relatively sensitive to hypoxia and does not survive deep hypoxia or anoxia. Given this lack of hypoxia-tolerance in the whole animal, the aim of this experiment was to investigate the in vitro responses of cultured rainbow trout cells following anoxia exposure. Rainbow trout hypodermal fibroblast (RTHDF) cells were exposed to anoxia for 12 and 24 h, whilst control cells were held under normoxic conditions for 24 h. Differential gene expression as a consequence of the treatments was analysed using an oligoarray composed of approximately 21,500 BLAST-identified sequences fabricated on the Agilent microarray platform. 57 genes were found to display significant responses to oxygen deprivation and these genes were assigned Gene Ontology terms and IDs. Of the 57 differentially expressed genes, 6 genes associated with carbohydrate metabolism were up-regulated following anoxia, these included phosphoglucomutase (PGM) and glycogen phosphorylase, consistent with glycogen serving as an important energy source during anoxia. Other genes up-regulated in response to anoxia included a number of putative targets of hypoxia inducible factor 1 alpha (HIF1A), namely phosphoglycerate kinase, triosephosphate isomerase and the glucose transporter, GLUT2. Egl9 homolog 3, the proline hydroxylase responsible for HIF1A regulation, was also induced. This analysis indicates that cultured trout cells have the capacity for adaptive gene responses when subjected to oxygen levels that are lethal to the whole organism.
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Project description:The environment inside even a small tumor is characterized by total (anoxia) or partial oxygen deprivation, hypoxia. It has been shown that radiotherapy and some conventional chemotherapies may be less effective in hypoxia, and therefore it is important to investigate how different drugs act in different microenvironments. In the associated study we performed a large screening of the effects of 19 clinically used or experimental chemotherapeutic drugs on four different cell lines in conditions of normoxia, hypoxia and anoxia. A panel of 19 commercially available drugs: 5-fluorouracil, acriflavine, bortezomib, cisplatin, digitoxin, digoxin, docetaxel, doxorubicin, etoposide, gemcitabine, irinotecan, melphalan, mitomycin c, rapamycin, sorafenib, thalidomide, tirapazamine, topotecan and vincristine were tested for cytotoxic activity on the cancer cell lines A2780 (ovarian), ACHN (renal), MCF-7 (breast), H69 (SCLC) and U-937 (lymphoma). Parallel aliquots of the cells were grown at different oxygen pressures and after 72 hours of drug exposure viability was measured with the fluorometric microculture cytotoxicity assay (FMCA). Sorafenib, irinotecan and docetaxel were in general more effective in an oxygenated environment, while cisplatin, mitomycin c and tirapazamine were more effective in a low oxygen environment. Surprisingly, hypoxia in H69 and MCF-7 cells mostly rendered higher drug sensitivity. In contrast ACHN appeared more sensitive to hypoxia, giving slower proliferating cells, and consequently, was more resistant to most drugs. Gene expression analysis was performed on MCF-7 cells after 90 hours in either anoxic or hypoxic conditions, and compared to cells grown in a regular cell incubator. The gene expression analysis was performed to validate that the cells were hypoxic/anoxic and showed the characteristic hypoxia response. Microarray based mRNA profiling was used to charactarize cells grown in hypoxia and anoxia. In the associated study we performed a large screening of the effects of 19 clinically used or experimental chemotherapeutic drugs on four different cell lines in conditions of normoxia, hypoxia and anoxia. We fin that hypoxia/anoxia render cancer cells both more resistant and more sensistive, depending of the type of drug used. The gene expression analysis was performed to validate that the cells really were hypoxic/anoxic and showed the characteristic hypoxia response. The cell line used for the gene expression analysis was MCF-7.
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Project description:Vascular disruption following bony injury results in a hypoxic gradient within the wound microenvironment. Nevertheless, the effects of low oxygen tension on osteogenic precursors remain to be fully elucidated. In the present study, we investigated in vitro osteoblast and mesenchymal stem cell differentiation following exposure to 21% O(2) (ambient oxygen), 2% O(2) (hypoxia), and <0.02% O(2) (anoxia). Hypoxia had little effect on osteogenic differentiation. In contrast, short-term anoxic treatment of primary osteoblasts and mesenchymal precursors inhibited in vitro bone nodule formation and extracellular calcium deposition. Cell viability assays revealed that this effect was not caused by immediate or delayed cell death. Microarray profiling implicated down-regulation of the key osteogenic transcription factor Runx2 as a potential mechanism for the anoxic inhibition of differentiation. Subsequent analysis revealed not only a short-term differential regulation of Runx2 and its targets by anoxia and hypoxia, but a long-term inhibition of Runx2 transcriptional and protein levels after only 12-24 h of anoxic insult. Furthermore, we present evidence that Runx2 inhibition may, at least in part, be because of anoxic repression of BMP2, and that restoring Runx2 levels during anoxia by pretreatment with recombinant BMP2 rescued the anoxic inhibition of differentiation. Taken together, our findings indicate that brief exposure to anoxia (but not 2% hypoxia) down-regulated BMP2 and Runx2 expression, thus inhibiting critical steps in the osteogenic differentiation of pluripotent mesenchymal precursors and committed osteoblasts.
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