Super-induced gene expression of the N-methyl-D-aspartate receptor 2C subunit in chemical-induced hypertrophic liver in rats

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Author(s)

    • ITO Sei
    • Department of Molecular Toxicology, School of Pharmaceutical Sciences, University of Shizuoka
    • MIZUKAMI Masanori
    • Department of Molecular Toxicology, School of Pharmaceutical Sciences, University of Shizuoka
    • HIKIDA Tokihiro
    • Department of Molecular Toxicology, School of Pharmaceutical Sciences, University of Shizuoka
    • GAMOU Toshie
    • Department of Pharmacodynamics and Molecular Genetics, School of Pharmacy, Iwate Medical University
    • HABANO Wataru
    • Department of Pharmacodynamics and Molecular Genetics, School of Pharmacy, Iwate Medical University
    • OZAWA Shogo
    • Department of Pharmacodynamics and Molecular Genetics, School of Pharmacy, Iwate Medical University
    • INOUE Kaoru
    • Division of Pathology, National Institute of Health Sciences
    • DEGAWA Masakuni
    • Department of Molecular Toxicology, School of Pharmaceutical Sciences, University of Shizuoka

Abstract

To identify gene expression that can be closely involved in chemical-induced hepatocellular hypertrophy, the hepatic gene expression profile was assessed by cDNA microarray analysis in male F344 rats fed for 3 days, 4 weeks, and 13 weeks a diet containing a hepatocellular hypertrophy inducer, either phenobarbital (500 ppm), clofibrate (2,500 ppm), or piperonyl butoxide (20,000 ppm). The results showed that, in all treatment groups, the increased expressional rate of the <i>Grin2c</i> gene, which encodes the <i>N</i>-methyl-D-aspartate receptor 2C subunit (NR2C), was the highest among those of all the genes tested, as compared with the corresponding gene expression in rats fed a normal diet. Moreover, real-time RT-PCR analysis showed that the expression levels of the <i>Grin2c</i> gene in rats fed with each chemical clearly increased in a chemical treatment period-dependent fashion, and that the increased rate was closely correlated with the grade of hypertrophy of hepatocytes rather than with the increased rate in liver weight. These results suggest the possibility that chemical-induced NR2C expression relates to the development of hepatocellular hypertrophy.

Journal

  • The Journal of Toxicological Sciences

    The Journal of Toxicological Sciences 36(5), 507-514, 2011-10-01

    The Japanese Society of Toxicology

References:  27

Cited by:  3

Codes

  • NII Article ID (NAID)
    10029481028
  • NII NACSIS-CAT ID (NCID)
    AN00002808
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    03881350
  • NDL Article ID
    11270365
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z19-1022
  • Data Source
    CJP  CJPref  NDL  J-STAGE 
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