title: Gene expression profile in chronic mouse liver injury caused by long-term exposure to CeCl3.
abstract: Numerous studies have demonstrated lanthanide (Ln) accumulation in the liver, and the corresponding damage; however, very little work has been done to evaluate the relationship between Ln-induced liver injury and its gene expression profile in mice. In this study, liver injury and gene-expressed profiles in male mice induced by oral administration of CeCl3 (2 mg/kg) via gavage for 90 consecutive days were investigated. The results showed that cerium accumulation, liver inflammation, and hepatocyte necrosis were observed. CeCl3 exposure significantly decreased the counts of white blood cells, lymphocyte, and platelet, the reticulocyte count (Ret) and neutrophilic granulocyte percentages as well as A/G ratio, whereas markedly increased the activities of alkaline phosphatase, lactate dehydrogenase, and cholinesterase, and the concentrations of triglycerides and total cholesterol. Furthermore, microarray results of liver showed that the differential expression of 675 known function genes involved in immune/inflammation response, apoptosis, metabolic process, cell cycle, cell proliferation, cytoskeleton, oxidative stress, signal transduction, transcription, translation, and transportation in CeCl3 exposed livers, respectively. Specifically, the significant downregulation of Nt5e led to inflammation, overexpressed Cyp4a12a and great suppression of Cdkn1a resulted in hepatocyte apoptosis, marked elevation of Cel, and Cyp7b1 expression caused the metabolic disorders in mouse liver after long-term CeCl3 exposure. Therefore, these genes may be in great relation to liver damages induced by exposure to CeCl3 .
authors.affiliation: Medical College, Soochow University, Suzhou 215123, People's Republic of China.
authors.forename: Jie
authors.initials: J
authors.lastname: Cheng
authors.forename: Min
authors.initials: M
authors.lastname: Fei
authors.forename: Min
authors.initials: M
authors.lastname: Fei
authors.forename: Xuezi
authors.initials: X
authors.lastname: Sang
authors.forename: Xuezi
authors.initials: X
authors.lastname: Sang
authors.forename: Zhe
authors.initials: Z
authors.lastname: Cheng
authors.forename: Suxin
authors.initials: S
authors.lastname: Gui
authors.forename: Xiaoyang
authors.initials: X
authors.lastname: Zhao
authors.forename: Lei
authors.initials: L
authors.lastname: Sheng
authors.forename: Qingqing
authors.initials: Q
authors.lastname: Sun
authors.forename: Renping
authors.initials: R
authors.lastname: Hu
authors.forename: Ling
authors.initials: L
authors.lastname: Wang
authors.forename: Fashui
authors.initials: F
authors.lastname: Hong
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics; D015415:Biomarkers / Q000378:metabolism; D002563:Cerium / Q000633:toxicity*; D004785:Environmental Pollutants / Q000633:toxicity*; D022781:Hepatocytes / Q000187:drug effects / Q000473:pathology; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008111:Liver Function Tests; D008297:Male; D008813:Mice, Inbred ICR; D018384:Oxidative Stress / Q000187:drug effects; D059467:Transcriptome
chemical_list: D015415:Biomarkers; D004785:Environmental Pollutants; D002563:Cerium; C026690:cerous chloride
keywords: cerium chloride; gene-expressed profile; liver dysfunction; liver injury