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ABSTRACT:
PROVIDER: PRJNA754198 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: Oxidative stress is thought to contribute to the development of age-related cataracts (ARCs), but the mechanisms by which oxidative damage leads to the opacification of the lens remain unclear. Previous studies suggest that oxidative stress can disrupt lens proteostasis. Therefore, it was hypothesized that ARCs arise from proteomic changes driven by an age-associated decline in oxidative stress defenses that interact with the lens proteostatic state. To test this hypothesis, proteomic analyses of lenses exposed to oxidative stress were performed to examine oxidative and proteostatic stress responses in vivo.Methods: Cataract formation was induced by injecting hydrogen peroxide into the aqueous humor of adult zebrafish. nrf2fh318/fh318 zebrafish were used to model the reduced oxidative stress protection observed in aged human lenses, while cryaba-/- zebrafish were used to model impaired lens proteostasis. Resulting opacities in WT, cryaba-/-, nrf2fh318/fh318, and cryaba-/-; nrf2fh318/fh318 lenses were quantified and proteomic changes in the cortex were analyzed using data independent acquisition Parallel Accumulation Serial Fragmentation mass spectrometry.Results: Hydrogen peroxide treatment induced the formation of cortical cataracts. Proteomic results showed that, dependent on genotype and day, oxidative stress activates the unfolded and mitochondrial unfolded protein responses. Additional changes were also observed in energy metabolism, Ca2+ homeostasis, protein degradation, and cytoskeletal and extracellular matrix remodeling pathways.Conclusions: Treated zebrafish lenses successfully model ARC and mass spectrometry proteomics identified the unfolded and mitochondrial unfolded protein responses as potential therapeutic targets for ARC.
2026-08-24 | PXD074656 | Pride
Project description:In this report, we have found that gata1 expressing erythroid cells contribute to a significant proportion of total body oxidative stress when animals were exposed to a strong pro-oxidant. RNA-seq of zebrafish under oxidative stress revealed the induction of tp53. Zebrafish carrying tp53 with mutation in its DNA binding domain were acutely sensitive to pro-oxidant exposure and displayed significant reactive oxygen species (ROS) and tp53-independent erythroid cell death resulting in an edematous phenotype. We found that a major contributing factor to ROS was increased basal mitochondrial respiratory rate without reserve. These data add to the concept that tp53, while classically a tumor suppressor and cell cycle regulator, has additional roles in controlling cellular oxidative stress.
2017-02-15 | GSE92754 | GEO
Project description:Contribution to the study of oxidative stress markers in laparoscopic vs open colectomy for colorectal cancer
| 2074362 | ecrin-mdr-crc
Project description:6PPD induces cerebrovascular defects by triggering oxidative stress and ferroptosis in zebrafish
| PRJNA1175041 | ENA
Project description:LysR-type transcriptional regulators (LTTRs) are emerging as key circuit components in regulating microbial stress responses and are implicated in modulating oxidative stress in the human opportunistic pathogen Pseudomonas aeruginosa. The oxidative stress response encapsulates several strategies to overcome the deleterious effects of reactive oxygen species. However, many of the regulatory components and associated molecular mechanisms underpinning this key adaptive response remain to be characterised. Comparative analysis of publically available transcriptomic datasets led to the identification of a novel LTTR, PA2206, whose expression was altered in response to a range of host signals in addition to oxidative stress. PA2206 was found to be required for tolerance to H2O2 in vitro and lethality in vivo in the Zebrafish embryo model of infection. Transcriptomic analysis in the presence of H2O2 showed that PA2206 altered the expression of 58 genes, including a large repertoire of oxidative stress and iron responsive genes, independent of the master regulator of oxidative stress, OxyR. Contrary to the classic mechanism of LysR regulation, PA2206 did not autoregulate its own expression and did not influence expression of adjacent or divergently transcribed genes. The PA2214-15 operon was identified as a direct target of PA2206 with truncated promoter fragments revealing binding to the 5M-bM-^@M-^Y-ATTGCCTGGGGTTAT-3M-bM-^@M-^Y LysR box adjacent to the predicted -35 region. PA2206 also interacted with the pvdS promoter suggesting a global dimension to the PA2206 regulon, and suggests PA2206 is an important regulatory component of P. aeruginosa adaptation during oxidative stress. Six samples were analysed in total, three biological replicates of the PA2206 mutant and PA2206 complemented strains. Each biological replicate included three technical replicates.
2013-01-01 | E-GEOD-23367 | biostudies-arrayexpress
Project description:Reactive oxygen species (ROS) within the retina play a key role in maintaining function and cell survival. However, excessive ROS can lead to oxidative stress, inducing dysregulation of metabolic and inflammatory pathways. The chmru848 zebrafish models choroideremia (CHM), an X-linked chorioretinal dystrophy which predominantly affects the photoreceptors, retinal pigment epithelium (RPE) and choroid. In this study, we examined the transcriptomic signature of the chmru848 zebrafish retina to reveal upregulation of cytokine pathways and glia migration, upregulation of oxidative, ER stress and apoptosis markers, and dysregulation of glucose metabolism with downregulation of glycolysis and upregulation of the oxidative phase of the pentose phosphate pathway. Glucose uptake was overall impaired in the chmru848 retina using the 2-NBDG glucose uptake assay, but after overexpression of human PFKM, it partially rescued the retinal phenotype and glucose uptake, but without modifying the expression of glycolysis markers. Therapies targeting glucose metabolism in CHM may represent a potential remedial approach.
2025-01-02 | GSE254948 | GEO
Project description:oxidative stress Methanoperedens nitroreducens
| PRJEB27089 | ENA