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CDDO drives transcriptomic and epigenetic reprogramming in response to TPA-induced JB6 cell neoplastic transformation [Methyl-seq]

ABSTRACT: CDDO drives transcriptomic and epigenetic reprogramming in response to TPA-induced JB6 cell neoplastic transformation [Methyl-seq]

PROVIDER: PRJNA849520 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19661976.fastq.gz	Fastqsanger.gz
	SRR19661977.fastq.gz	Fastqsanger.gz
	SRR19661978.fastq.gz	Fastqsanger.gz

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CDDO drives transcriptomic and epigenetic reprogramming in response to TPA-induced JB6 cell neoplastic transformation [Methyl-seq]

Project description:12-O-tetradecanoylphorbol-13-acetate (TPA) promotes skin carcinogenesis. CDDO is a potential antioxidative and antiinflammatory agent to prevent the TPA-induced skin cell transformation at nanomolar scale. We characterized the transcriptome, CpG methylome, and pathway network of JB6 cells treated with TPA and TPA + CDDO using RNA sequencing, methyl sequencing, and QIAGEN Ingenuity Pathway Analysis.

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Project description:CDDO drives transcriptomic and epigenetic reprogramming in response to TPA-induced JB6 cell neoplastic transformation

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CDDO drives transcriptomic and epigenetic reprogramming in response to TPA-induced JB6 cell neoplastic transformation

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Bardoxolone methyl improves nonalcoholic steatohepatitis through inhibition of macrophage recruitment

Project description:Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease caused by excess fat accumulation, closely associated with obesity and metabolic syndrome.Bardoxolone methyl (2-Cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid methyl ester, CDDO-Me) is a potent activator of nuclear factor erythroid 2-related factor 2 (Nrf2). Some clinical trials of CDDO-Me were conducted for chronic kidney diseases and pulmonary arterial hypertension, whereas the hepatoprotective effect of CDDO-Me on nonalcoholic steatohepatitis (NASH) has not yet been elucidated. The purpose of this study was to determine the hepatoprotective potential and mechanisms of CDDO-Me in a diet-induced NASH mouse model. Whole transcriptome analysis revealed that CDDO-Me markedly inhibited the expressions of chemokine ligands, Ccl3 and Ccl4, and the chemokine receptors, Ccr1 and Ccr5 that increased in NASH mice while activating Nrf2-dependent pathway. Serum protein levels of CCL3 and CCL4 upregulated in NASH mice were inhibited in a dose-dependent manner by treatment with CDDO-Me. CDDO-Me inhibited the expression levels of Ccr1 and Ccr5, and simultaneously blocked Ccl3 and Ccl4 the ligands of the receptors, respectively in RAW264.7 cell line. Taken together with the observations, CDDO-Me directly inhibits the expression of CCL3-CCR1 and CCL4-CCR5 axes in macrophages of NASH mice, which might contribute to the improvement of nonalcoholic steatohepatitis and fibrosis through the interference of monocyte-derived macrophage migration.

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Expression profiling by array in livers of Nrf2 null mice administered CDDO-IM

Project description:Nrf2 null mice administered CDDO-IM Nrf2 null mice treated with CDDO-IM

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