Dataset Information

Proteomic analysis of mPGES-2 on NAFLD

ABSTRACT: Proteomic analysis was performed using LC-MS/MS technology from Shanghai Aiao Biotechnology Co., Ltd.. The abundance of peptide fractions in the livers of Ptges2+/+ (WT) HFD and Ptges2-/- (KO) HFD groups was quantified using unlabeled quantitative methods and differentially expressed proteins in each group were tested for significance using t-test.

ORGANISM(S): Mus Musculus

SUBMITTER: Ying Sun

PROVIDER: PXD035389 | iProX | Tue Jul 19 00:00:00 BST 2022

REPOSITORIES: iProX

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Publications

Inhibition of mPGES-2 ameliorates NASH by activating NR1D1 via heme.

Zhong Dandan D Cai Jie J Hu Cheng C Chen Jingshuo J Zhang Rumeng R Fan Chenyu C Li Shanshan S Zhang Hongxing H Xu Zhou Z Jia Zhanjun Z Guo Dong D Sun Ying Y

Hepatology (Baltimore, Md.) 20220808 2

<h4>Background and aims</h4>Nonalcoholic fatty liver disease (NAFLD), a complex metabolic syndrome, has limited therapeutic options. Microsomal prostaglandin E synthase-2 (mPGES-2) was originally discovered as a prostaglandin E 2 (PGE 2 ) synthase; however, it does not produce PGE 2 in the liver. Moreover, the role of mPGES-2 in NAFLD remains undefined. Herein, we aimed to determine the function and mechanism of mPGES-2 in liver steatosis and steatohepatitis.<h4>Approach and results</h4>To evalu ...[more]

PMID: 35839302

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Project description:Chronic liver inflammation precedes the majority of hepatocellular carcinomas (HCC). Here, we explore the connection between chronic inflammation and DNA methylation in the liver at the late precancerous stages of HCC development in Mdr2/Abcb4-knockout (Mdr2-KO) mice, a model of inflammation-mediated HCC. Using methylated DNA immunoprecipitation (MeDIP) followed by hybridization with Agilent CpG Islands (CGIs) microarrays we found specific CGIs in 76 genes which were hypermethylated in the Mdr2-KO liver compared to age-matched controls. Methylation of thirty among these genes was highly specific to the studied HCC model. We revealed that in most tested cases, the observed hypermethylation resulted from an age-dependent decrease of methylation of the specific CGIs in control livers with no decrease in mutant mice. Chronic inflammation did not change global levels of DNA methylation in Mdr2-KO liver, but caused a 2-fold decrease of the global 5-hydroxymethylcytosine level in mutants compared to controls. This decrease could result from a less efficient age-dependent demethylation of specific CpG sites in the liver of Mdr2-KO mutants, as described above. Expression of some tested hypermethylated genes was increased in Mdr2-KO livers compared to controls (28%), others were either similarly expressed (44%), or not expressed in the liver (28%). Liver cell fractionation revealed, that the relative hypermethylation of specific CGIs in Mdr2-KO compared to control livers affected either hepatocyte, or non-hepatocyte, or both fractions. There was only episodic correlation between changes of gene methylation and expression in cell fractions. Conclusion: Chronic liver inflammation causes hypermethylation of specific CGIs, which may affect both hepatocytes and non-hepatocyte liver cells. These changes may serve as markers of an increased regenerative activity and of a precancerous microenvironment in the chronically inflamed liver. Two-condition experiment, Mdr2-KO vs Mdr2-/+ liver tissue from 12m-old male FVB strain mice. Biological replicates: 3 control replicates, 3 knockout replicates.

Dataset Information

Proteomic analysis of mPGES-2 on NAFLD

Publications

Inhibition of mPGES-2 ameliorates NASH by activating NR1D1 via heme.

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