Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA294322 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Lactobacilli modulate epithelial cytoprotection through the Nrf2 pathway
| PRJNA294320 | ENA
Project description:Lactobacilli modulate epithelial cytoprotection through the Nrf2 pathway [RNA-Seq]
| PRJNA294323 | ENA
Project description:The intestinal ecosystem is balanced by dynamic interactions between resident and incoming microbes, the gastrointestinal barrier, and the mucosal immune system. However, in the context of inflammatory bowel diseases (IBD) where the integrity of the gastrointestinal barrier is compromised, resident microbes contribute to the development and perpetuation of inflammation and disease. In this context, probiotic bacteria exert beneficial effects enhancing epithelial barrier integrity. However, the mechanisms underlying these beneficial effects are only poorly understood. Here, we comparatively investigated the effects of four probiotic lactobacilli, namely L. acidophilus, L. fermentum, L. gasseri, and L. rhamnosus in a T84 cell epithelial barrier model. Results of DNA-microarray experiments indicating that lactobacilli modulate the regulation of genes encoding in particular adherence junction proteins such as E-cadherin and b-catenin were confirmed by qRT-PCR. Furthermore, we show that epithelial barrier function is modulated by Gram-positive probiotic lactobacilli via their effect on adherence junction protein expression and complex formation. In addition, incubation with lactobacilli differentially influences the phosphorylation of adherence junction proteins and of PKC isoforms such as PKCd which thereby positively modulates epithelial barrier function. Further insight into the underlying molecular mechanisms triggered by these probiotics might also foster the development of novel strategies for the treatment of gastrointestinal diseases (e.g. IBD).
2012-02-10 | E-MEXP-3445 | biostudies-arrayexpress
Project description:Drosophila elevated CO2 (hypercapnia) microarray
| PRJNA118867 | ENA
Project description:Logjam p24 mutant microarray analysis
| PRJNA107253 | ENA
Project description:Drosophila CNS OXPHOS inhibition microarray
| PRJNA379770 | ENA
Project description:The BTB-zinc finger transcription factor Abrupt acts as an epithelial oncogene in Drosophila through maintaining a progenitor-like cell state
| PRJNA183883 | ENA
Project description:In inflammatory diseases of the airway, a high level (estimated to be as high as 8 mM) of HOCl can be generated through a reaction catalyzed by the leukocyte granule enzyme myeloperoxidase (MPO). HOCl, a potent oxidative agent, causes extensive tissue injury through its reaction with various cellular substances, including thiols, nucleotides, and amines. In addition to its physiological source, HOCl can also be generated by chlorine gas inhalation from an accident or a potential terrorist attack. Despite the important role of HOCl-induced airway epithelial injury, the underlying molecular mechanism is largely unknown. In the present study, we found that HOCl induced dose-dependent toxicity in airway epithelial cells. By transcription profiling using GeneChip, we identified a battery of HOCl-inducible antioxidant genes, all of which have been reported previously to be regulated by nuclear factor erythroid-related factor 2 (Nrf2), a transcription factor that is critical to the lung antioxidant response. Consistent with this finding, Nrf2 was found to be activated time and dose dependently by HOCl. Although the epidermal growth factor receptor-MAPK pathway was also highly activated by HOCl, it was not involved in Nrf2 activation and Nrf2-dependent gene expression. Instead, HOCl-induced cellular oxidative stress appeared to lead directly to Nrf2 activation. To further understand the functional significance of Nrf2 activation, small interference RNA was used to knock down Nrf2 level by targeting Nrf2 or enhance nuclear accumulation of Nrf2 by targeting its endogenous inhibitor Keap1. By both methods, we conclude that Nrf2 directly protects airway epithelial cells from HOCl-induced toxicity. Experiment Overall Design: This is genechip study. Detailed study design is described in: Am J Physiol Lung Cell Mol Physiol. 2008 Mar;294(3):L469-77. Epub 2007 Dec 21.
2008-06-18 | E-GEOD-11630 | biostudies-arrayexpress
Project description:CLAMP Protein Binding Microarray (PBM) experiment
| PRJNA325941 | ENA