Dataset Information

Proteomics analysis of different stages during mouse hepatic ischemia-reperfusion injury

ABSTRACT: 6-plex TMT-based quantitative proteomics was used to analysis the proteomic profile in different stages of mouse hepatic ischemia-reperfusion injury.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: Yanfang Su

LAB HEAD: Hongliang Li

PROVIDER: PXD007827 | Pride | 2017-11-23

REPOSITORIES: Pride

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			Action	DRS
	20160413-LHL-TMT1-Frac0.raw	Raw
	20160413-LHL-TMT1-Frac1.raw	Raw
	20160413-LHL-TMT1-Frac2.raw	Raw
	20160413-LHL-TMT1-Frac3.raw	Raw
	20160413-LHL-TMT1-Frac4.raw	Raw

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Publications

An ALOX12-12-HETE-GPR31 signaling axis is a key mediator of hepatic ischemia-reperfusion injury.

Zhang Xiao-Jing XJ Cheng Xu X Yan Zhen-Zhen ZZ Fang Jing J Wang Xiaozhan X Wang Weijun W Liu Zhen-Yu ZY Shen Li-Jun LJ Zhang Peng P Wang Pi-Xiao PX Liao Rufang R Ji Yan-Xiao YX Wang Jun-Yong JY Tian Song S Zhu Xue-Yong XY Zhang Yan Y Tian Rui-Feng RF Wang Lin L Ma Xin-Liang XL Huang Zan Z She Zhi-Gang ZG Li Hongliang H

Nature medicine 20171211 1

Hepatic ischemia-reperfusion (IR) injury is a common clinical issue lacking effective therapy and validated pharmacological targets. Here, using integrative 'omics' analysis, we identified an arachidonate 12-lipoxygenase (ALOX12)-12-hydroxyeicosatetraenoic acid (12-HETE)-G-protein-coupled receptor 31 (GPR31) signaling axis as a key determinant of the hepatic IR process. We found that ALOX12 was markedly upregulated in hepatocytes during ischemia to promote 12-HETE accumulation and that 12-HETE t ...[more]

PMID: 29227475

Similar Datasets

Project description:Experimental Design: 1. The goal of the experiment: Age-Dependent Gene Expression Profiles After Hepatic Ischemia/Reperfusion: Implications for the AP-1 and Ubiquitin-Proteosome Pathways 2. Brief description of the experiment: Hepatic ischemia/reperfusion (I/R) injury is a complication of liver surgery, transplantation and shock. Our previous studies have suggested there is an age-dependent response to I/R. In the present study, we examined global gene expression after liver I/R in young (4-5 weeks) and adult (12-14 months) mice using Affymetrix microarray. Gene expression was filtered based on a change in expression of 1.5-fold relative to respective controls and then analyzed by ANOVA. Seventy-two genes in young mice and 56 genes in adult mice had significantly increased expression. Of these, only 18 were up-regulated in both age groups. In young mice, 289 genes were down-regulated whereas in adult mice, 874 genes were decreased. Of these genes, 175 genes were decreased in both groups. Pathway and network analyses of up- and down-regulated gene lists revealed a number of notable differences between young and adult mice. Of these, we found that genes related to the activating protein-1 (AP-1) pathway were upregulated preferentially in young mice. This corresponded with an increase in AP-1 activation in young versus adult mice. Finally, we found that genes related to the ubiquitin-proteasome pathway were selectively down-regulated in adult mice. This was accompanied by reduced degradation of the inhibitory protein, I?B?, in adult mice. The data demonstrate specific, pathway- and network-related differences in gene expression profiles between young and adult mice in the response to I/R. More specifically, we have identified two pathways that may contribute to the superior response to I/R in young mice which represent potential therapeutic targets. Keywords: treated vs non treated 2 age groups of 6 young and 6 adult mice that underwent either 90 minutes of partial ischemia followed by 1 hour of reperfusion (n=3) or sham operation (n=3) We used microarray to uncover the genomic response after ischemia reperfusion in 2 different age groups