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Long-term exposure to PM2.5 aggravates pulmonary fibrosis and acute lung injury by disrupting Nrf2-mediated antioxidant function

ABSTRACT: Long-term exposure to PM2.5 aggravates pulmonary fibrosis and acute lung injury by disrupting Nrf2-mediated antioxidant function

PROVIDER: PRJNA851832 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19787048.fastq.gz	Fastqsanger.gz
	SRR19787049.fastq.gz	Fastqsanger.gz
	SRR19787050.fastq.gz	Fastqsanger.gz
	SRR19787051.fastq.gz	Fastqsanger.gz
	SRR19787052.fastq.gz	Fastqsanger.gz

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Long-term exposure to PM2.5 aggravates pulmonary fibrosis and acute lung injury by disrupting Nrf2-mediated antioxidant function

Project description:To investigate the difference damage patterns bewteen short-term and long-term exposure to PM2.5 particulate matter

2022-06-24 | GSE206733 | GEO

Activation of Nrf2/HO-1 signaling pathway exacerbates cholestatic liver injury

Project description:Nrf2 antioxidant signaling is involved in liver protection, but this generalization overlooks conflicting studies indicating that Nrf2 effects are not necessarily hepatoprotective. The role of Nrf2/HO-1 in cholestatic liver injury (CLI) remains poorly defined. Here, we report that Nrf2/HO-1 activation exacerbates liver injury rather than exerts a protective effect in CLI. Inhibiting HO-1 or ameliorating bilirubin transport alleviates liver injury in CLI models. Nrf2 knockout confers hepatoprotection in CLI mice, whereas in non-CLI mice, Nrf2 knockout aggravates liver damage. In the CLI setting, oxidative stress activates Nrf2/HO-1, leads to bilirubin accumulation, and impairs mitochondrial function. High levels of bilirubin reciprocally upregulate the activation of Nrf2 and HO-1, while antioxidant and mitochondria-targeted SOD2 overexpression attenuate the toxicity of bilirubin. Additionally, the expression of Nrf2 and HO-1 is significantly elevated in serum of patients with CLI. These results reveal an unrecognized function of Nrf2 signaling in exacerbating liver injury in cholestatic disease.

2024-04-08 | GSE263093 | GEO

Transcription profiling of wild type and Nrf2 knock out treated with 100% oxygen to induce lung injury mice to provide insight to the downstream effector genes regulated by Nrf2

Project description:Nrf2 is a transcription factor that binds to antioxidant response elements of the regulatory region of a number of antioxidant genes. A mutation in the Nrf2 gene increases susceptibility to hyperoxic lung injury. This project examines expression differences between wild type and Nrf2 knock out mice with the hope of providing insight to the downstream effector genes regulated by Nrf2.

2007-12-14 | E-GEOD-495 | biostudies-arrayexpress

Pereira2020 - NRF2–p53 integrated-systems model of oxidative stress

Project description:Integrated-systems model of oxidative stress connecting NRF2 and p53 signaling pathways. Additional crosstalk linking oxidative stress to p53 inhibition, p53 to NRF2 through p21, and NRF2 to MDM2 was incorporated in this model. The NRF2 pathway was encoded as first- and second-order rate equations for KEAP1 oxidation and NRF2 stabilization; NRF2-mediated transcription of antioxidant enzymes was modeled as a Hill function. The p53 pathway was reconstructed from a delay differential equation model of p53 signaling in response to DNA damage. To adapt the p53 DNA-damage model to respond to oxidative stress, we used a first-order oxidation reaction of ATM/CHEK2 by intracellular H2O2. The integrated base model of NRF2–p53 oxidative-stress signaling contains 42 reactions and 22 ordinary differential equations (ODEs).

2021-10-29 | MODEL2110270001 | BioModels

Gene expression profiles in livers caused by Atg7 and/or Nrf2 deficiency

Project description:Autophagy deficiency caused by conditional knockout of Atg7 results in severe hepatitis accompanied by abundant accumulation of p62. p62 stablizes Nrf2 by disrupting the association between Keap1 and Nrf2. To understand the pathogenesis of hepatitis under the autophagy deficiency, we examined gene expression profiles of livers from Atg7-null, Nrf2-null and Atg7-Nrf2 double mutant mice. Eight week old Atg7F/F:Mx1-Cre mice and Atg7F/F:Mx1-Cre:Nrf2-/- together with control mice were injected with pIpC. At 4 weeks after pIpC injection, total RNAs were purified from each mouse liver.

2010-10-14 | E-GEOD-20415 | biostudies-arrayexpress

Effect of liver-specific deletion of Gclc, Nrf2, and Gclc-Nrf2 on the liver

Project description:The rate-limiting step in glutathione (GSH) synthesis is controlled by glutamate-cysteine ligase catalytic subunit. GSH is reported to buffer oxidative stress. In the absence of GSH, the antioxidant transcription factor Nrf2 is reported to be stabilized. The liver has the highest levels of GSH, but its impact on liver homeostasis is unclear. To investigate this, we induced a liver-specific deletion of Gclc (Gclc f/f), Nrf2 (Nrf2 f/f), or Gclc-Nrf2 (Gclc f/f Nrf2 f/f) by injecting my via tail-vein with AAV-TBG-Cre, which induces recombination specifically in hepatocytes.

2024-05-29 | GSE263119 | GEO

RNA-seq analysis of NRF2 silenced human skin fibroblasts

Project description:This RNA-seq analysis was the beginning of our study, to have a first global unbiased approach to analyze the effect of NRF2 silencing on the mRNA profile of human skin fibroblasts. We demonstrated that besides NRF2 conventional antioxidant and metabolic target genes, tissue skeleton and especially matrisome genes were affected by NRF2 silencing. We further confirmed that NRF2 silencing some collagen genes, impacting collagen fibrillogenesis.

2022-06-01 | GSE185129 | GEO

Functional analysis of the cytoprotective transcription factor Nrf2 in skin morphogenesis and disease: Identification of Nrf2 target genes

Project description:The Nrf2 transcription factor is a key player in the cellular stress response, which regulates the expression of important antioxidant enzymes and other cytoprotective proteins. We recently generated a novel transgenic mouse model to determine the function of Nrf2 in the skin. These mice revealed interesting phenotypic abnormalities, including hyperkeratosis and acanthosis. To gain insight into the underlying molecular mechanisms, we wanted to identify genes, which are differentially expressed in the skin of wild-type and mutant mice before the onset of phenotypic abnormalities. RNA from whole skin of 3 single P2.5 K5cre-caNrf2 (tg/tg) and 3 single P2.5 K5cre-wt (tg/wt=control) mice were used

2012-02-01 | E-GEOD-35160 | biostudies-arrayexpress

Nrf2 transcript alterations

Project description:WGS and RNA-seq data for Nrf2 study

| EGAS00001001740 | EGA

Transcriptomic approach to renal toxicity for cisplatin treatment in Nrf2 WT/KO

Project description:NF-E2-related factor 2 (Nrf2), a transcription factor activated by oxidative stress, induces phase II conjugating or antioxidant enzymes. In the present study, we examined the effect of Nrf2 knockout (Nrf2 KO) on the kidney injury induced by cisplatin using cDNA microarray analyses. A transcriptomic approach enabled us to extract gene clusters which show significantly different mRNA expression patterns between wild type (WT) and Nrf2 KO mice. In the experimental set, WT vehicle (WT-Veh) and WT cisplatin (WT-Cis) groups were included in our previous GEO database (GSE35257) because the two groups were simultaneously shared with Nrf2 KO vehicle (Nrf2 KO-Veh) and Nrf2 KO cisplatin (Nrf2 KO-Cis) groups in the current report. Copyright (c) 2012 by Korea Food & Drug Administration. WT and Nrf2 KO C57BL/6 mice (9 weeks old, male) were intraperitoneally injected with vehicle (saline) or a single dose of cisplatin (15 mg/kg body weight). The cDNA microarray experiments were done for the kidney of mice 3 days after treatment. Three animals were used per group. WT-Veh and WT-Cis groups were already deposited in GSE35257.

2014-01-01 | E-GEOD-48879 | biostudies-arrayexpress

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