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Time- and dose-based gene expression profiles produced by a bile-duct-damaging chemical, 4,4′-methylene dianiline, in mouse liver in an acute phase

Title
Time- and dose-based gene expression profiles produced by a bile-duct-damaging chemical, 4,4′-methylene dianiline, in mouse liver in an acute phase
Authors
Kwon S.-B.Park J.-S.Yi J.-Y.Hwang J.-W.Kim M.Lee M.-O.Lee B.-H.Kim H.-L.Kim J.H.Chung H.Kong G.Kang K.-S.Yoon B.-I.
Ewha Authors
김형래
SCOPUS Author ID
김형래scopus
Issue Date
2008
Journal Title
Toxicologic Pathology
ISSN
0192-6233JCR Link
Citation
vol. 36, no. 5, pp. 660 - 673
Indexed
SCIE; SCOPUS WOS scopus
Abstract
A toxicogenomics study was performed in the mouse liver after treatment of a bile-duct-damaging chemical, 4,4′-methylene dianiline (MDA), across multiple doses and sampling times in an acute phase using the AB Expression Array System. Imprinting control region (ICR) mice were given a single oral administration of a low (10 mg/kg b.w.) or high (100 mg/kg b.w.) dose of MDA. Mice were sacrificed six, twenty-four, and seventy-two hours after treatment for serum chemistry, histopathology, and mRNA preparation from liver samples. Treatment with MDA increased liver-toxicity-related enzymes in blood and induced bile-duct cell injury, followed by regeneration. To explore potential biomarker gene profiles, the altered genes were categorized into four expression patterns depending on dose and time. Numerous functionally defined and unclassified genes in each category were up- or down-regulated throughout the period from cellular injury to the recovery phase, verified by RT-PCR. Many genes associated with liver toxicity and diseases belonged to one of these categories. The chemokine-mediated Th1 pathway was implicated in the inflammatory process. The genes associated with oxidative stress, apoptosis, and cell-cycle regulation were also dynamically responsive to MDA treatment. The Wnt/β-catenin signaling pathway was likely responsible for the reconstitution process of the MDA-injured liver. Copyright © 2008 by Society of Toxicologic Pathology.
DOI
10.1177/0192623308320272
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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