title: Lipid metabolism and peroxisome proliferator-activated receptor signaling pathways participate in late-phase liver regeneration.
abstract: Liver regeneration (LR) is of great clinical significance in various liver-associated diseases. LR proceeds along a sequence of three distinct phases: priming/initiation, proliferation, and termination. Compared with the recognition of the first two phases, little is known about LR termination and structure/function reorganization. A combination of "omics" techniques, along with bioinformatics, may provide new insights into the molecular mechanism of the late-phase LR. Gene, protein, and metabolite profiles of the rat liver were determined by cDNA microarray, two-dimensional electrophoresis, and HPLC-MS analysis. Pathway enrichment analysis was performed to identify the pathways: 427 differentially expressed genes extracted from the microarray experiment revealed two expression patterns representing the early and late phase of LR. Functionally, the genes expressing at a higher level at the early phase than at the late phase were mainly involved in the response to stress, proliferation, and resistance to apoptosis, while those expressing at a lower level at the early phase than at the late phase were mainly engaged in lipid metabolism. Compared with the sham-operation control (SH) group, 5 proteins in the 70% partial hepatectomy (70%PHx) group were upregulated at the protein level, and 3 proteins were downregulated at 168 h after the 70%PHx. E-FABP, an upregulated fatty acid binding protein, was found to be involved in the peroxisome proliferator-activated receptor (PPAR) signaling pathway. The metabolomic data confirmed the enhancement of lipid metabolism by the detection of the intermediate and final metabolites. We've concluded that increased lipid metabolism and activated PPAR signaling pathways play important roles in late-phase LR.
authors.affiliation: Department of Biochemistry and Molecular Biology, Second Military Medical University, Shanghai 200433, People's Republic of China.
authors.forename: Xing
authors.initials: X
authors.lastname: Yuan
authors.forename: Shikai
authors.initials: S
authors.lastname: Yan
authors.forename: Jing
authors.initials: J
authors.lastname: Zhao
authors.forename: Duo
authors.initials: D
authors.lastname: Shi
authors.forename: Bin
authors.initials: B
authors.lastname: Yuan
authors.forename: Weixing
authors.initials: W
authors.lastname: Dai
authors.forename: Binghua
authors.initials: B
authors.lastname: Jiao
authors.forename: Weidong
authors.initials: W
authors.lastname: Zhang
authors.forename: Mingyong
authors.initials: M
authors.lastname: Miao
mesh_terms: D000818:Animals; D020869:Gene Expression Profiling / Q000379:methods; D050356:Lipid Metabolism; D008099:Liver / Q000502:physiology; D008107:Liver Diseases / Q000378:metabolism; D008115:Liver Regeneration / Q000502:physiology*; D008297:Male; D013058:Mass Spectrometry / Q000379:methods; D046228:Microarray Analysis; D047492:Peroxisome Proliferator-Activated Receptors / Q000378:metabolism*; D020543:Proteome / Q000032:analysis; D040901:Proteomics / Q000379:methods; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D047492:Peroxisome Proliferator-Activated Receptors; D020543:Proteome