Unknown,Transcriptomics,Genomics,Proteomics

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Meythlation profiling by array to investigate the effect of hyperoxia on DNA methylation in mouse lung tissue

ABSTRACT: Hyperoxia has a potential to alter DNA methylation status. We assessed the effect of long term hyperoxia in mouse lung tissue. A total of 24 mice were randomized to hyperoxia (85% O2; 12 animals) or normoxia (21% O2; 12 animals) for 14 days continued with normoxia conditions for all animals for the subsequent 14 days. All mice had free access to food and water and were kept under standard conditions in A-Chambers (O2 – monitor ProOX110, CO2 – monitor ProCO2 P120, BioSpherix). The animals were sacrificed on day 28. Lung tissue was harvested on day 28 after euthanasia with a zolazepam/tiletamine/xylazine/fentanyl cocktail. Tissues samples were snap-frozen in liquid nitrogen immediately after cessation of circulation for the subsequent analysis. Subsequently, DNA methylation profiles in lung tissue were compared by means of methylation microarrays between both groups. We used the Genomic Workbench software (Agilent) to assess the mean methylation status of each DNA fragment (array probe) in each group. We first calculated the normalised, combined Z-scores, representing summation of the left and right Gaussian Z-scores and reflecting the location of a probe log-ratio value in relation to the Gaussian distribution of probes. A strong positive value of the combined Z-score means that a given probe is methylated and strong negative value means that it is unmethylated. Next, we compared the mean combined Z-scores (average methylation patterns) of the probes between hyperoxia and normoxia groups.

ORGANISM(S): Mus musculus

SUBMITTER: Miroslaw Bik-Multanowski

PROVIDER: E-MTAB-6489 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

MTRNR2L12: A Candidate Blood Marker of Early Alzheimer's Disease-Like Dementia in Adults with Down Syndrome.

Bik-Multanowski Miroslaw M Pietrzyk Jacek J JJ Midro Alina A

Journal of Alzheimer's disease : JAD 20150101 1

Morphological abnormalities observed typically in the brains of adults with Down syndrome are identical with those present in patients with Alzheimer's disease. However, only some adults with Down syndrome suffer from early dementia, whereas others remain unaffected. We aimed to identify the genomic background responsible for this observation. We performed cognitive assessment and genome expression analysis of blood mononuclear cells in seniors with Down syndrome. Unaffected elderly patients and ...[more]

PMID: 25720405

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Project description:Background: Nrf2 is an essential cytoprotective transcription factor. However, association of Nrf2 in organ development and neonatal disease is rarely examined. Hyperoxia exposure to newborn rodents generates pulmonary phenotypes which resemble bronchopulmonary dysplasia (BPD) of prematurity. Methods: To investigate the role of Nrf2 in lung maturation and BPD pathogenesis, Nrf2-deficient (Nrf2-/-) and wild-type (Nrf2+/+) neonates were exposed to air or hyperoxia (O2). Transcriptome analysis determined Nrf2-directed mechanisms in premature lung. Lung injury was assessed by bronchoalveolar lavage analysis and histopathology. Results: In Nrf2-/- neonates, basal expression of cell cycle machinery, redox balance, and lipid/carbohydrate metabolism genes were suppressed while immunity genes were overexpressed compared to Nrf2+/+ pups. O2-induced mortality and pulmonary inflammation/injury were significantly higher in Nrf2-/- than in Nrf2+/+. Lung DNA lesion and oxidation were greater in Nrf2-/- than in Nrf2+/+, constitutively and after O2. Nrf2-dependent genes modulated cellular growth/proliferation, defense, immunity, and lipid metabolism against hyperoxia. Bioinformatic elucidation of Nrf2 binding motifs and augmented O2-induced inflammation in genetically deficient neonates validated Gpx2 and Marco as Nrf2 effectors. Conclusion: Overall, Nrf2 in underdeveloped lungs orchestrated cell cycle, morphogenesis, and immunity as well as cellular defense constitutively and under oxidant stress. Results provide putative molecular mechanisms of Nrf2-directed lung alveolarization and BPD of prematurity. PARALLEL study design with 42 samples comparing 14 groups of age (P1 to P4 corresponding to day 0 to day 3 animals), gene, and exposure: (4 groups Nrf+/+ wild type P1-P4 air exposure) (4 groups Nrf -/- knockout P1-P4 air exposure), (3 groups Nrf+/+ wild type P2-P4 with 100 percent O2 (hyperoxia exposure) and 3 groupsNrf -/- knockout P2-P4 with 100 percent O2 (hyperoxia exposure)) Biological replicates: 3 per group

Dataset Information

Meythlation profiling by array to investigate the effect of hyperoxia on DNA methylation in mouse lung tissue

Publications

MTRNR2L12: A Candidate Blood Marker of Early Alzheimer's Disease-Like Dementia in Adults with Down Syndrome.

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