Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression profile of cortices, hippocampi and brainstems of Nrf2 knockout mice under unstressed conditions

ABSTRACT: Microarray analysis of cortices, hippocampi and brainstems of Nrf2 knockout mice, Three independent RNAs from cortices, hippocampi and brainstems of Nrf2 knockout and wild-type control mice were used for the microarray analyses.

ORGANISM(S): Mus musculus

SUBMITTER: Masayuki Yamamoto

PROVIDER: E-GEOD-47587 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Nrf2 deficiency leads to behavioral, neurochemical and transcriptional changes in mice.

Muramatsu Hiroyuki H Katsuoka Fumiki F Toide Katsuo K Shimizu Yusuke Y Furusako Shoji S Yamamoto Masayuki M

Genes to cells : devoted to molecular & cellular mechanisms 20130729 10

Nrf2 is a transcription factor that regulates the antioxidant and detoxification enzyme genes and provides defense against oxidative and electrophilic stresses in various tissues. In brain, while neuroprotective functions of Nrf2 have been well documented, Nrf2 contribution to the brain function remains to be elucidated. To address this issue, we investigated whether Nrf2 deficiency affects psychological behaviors, neurotransmitter systems and gene expressions in mice. We conducted four behavior ...[more]

PMID: 23890231

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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

Expression profile of cortices, hippocampi and brainstems of Nrf2 knockout mice under unstressed conditions

Publications

Nrf2 deficiency leads to behavioral, neurochemical and transcriptional changes in mice.

Similar Datasets

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