TA1 oncofetal rat liver cDNA and putative amino acid permease:: Temporal correlation with c-myc during acute CCl4 liver injury and variation of RNA levels in response to amino acids in hepatocyte cultures

被引:11
作者
Shultz, VD [1 ]
Campbell, W [1 ]
Karr, S [1 ]
Hixson, DC [1 ]
Thompson, NL [1 ]
机构
[1] Brown Univ, Sch Med, Rhode Isl Hosp, Dept Med Oncol, Providence, RI 02912 USA
关键词
carbon tetrachloride; liver regeneration; acute liver injury; partial hepatectomy; amino acids; hepatocytes; adaptive regulation;
D O I
10.1006/taap.1998.8555
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
TA1 is a rat liver oncofetal cDNA and a member of an emerging family of evolutionarily conserved molecules with homology to amino acid transporters and permeases. The aim of these studies was to characterize the regulation and role of TA1 in acute rat liver injury by examining its relation to regeneration and metabolic stress. Following a single dose of CCl4, TA1 message was expressed 3-48 h. The major 3.3-kb TA1 transcript correlated temporally with c-myc expression. A novel 2.9-kb TA1 transcript was expressed more variably 24-48 h. TA1 protein was restricted to hepatocytes in G(0) and G(1) phases of the cell cycle. Relative to CCl4, a much smaller increase in TA1 was noted after partial hepatectomy and TA1 preceded the peak of c-myc expression. In vitro TA1 was not induced in hepatocytes by EGF or the acute-phase cytokines IL-6 and TNF-alpha, but was found to be modulated in response to amino acid availability. TA1 expression increased in media without arginine and glutamine and was repressed by total amino acid levels 5-fold over basal MEM. Together, these results contrast with the constitutive expression observed in transformed cells and suggest an adaptive role for TA1 during liver injury. (C) 1999 Academic Press.
引用
收藏
页码:84 / 96
页数:13
相关论文
共 48 条
  • [1] BRAND HS, 1995, J HEPATOL, V23, P333
  • [2] CACCIATORE L, 1973, RES COMMUN CHEM PATH, V6, P473
  • [3] Role of nutrition in the survival after hepatotoxic injury
    Chanda, S
    Mehendale, HM
    [J]. TOXICOLOGY, 1996, 111 (1-3) : 163 - 178
  • [4] ISOLATION OF BIOLOGICALLY-ACTIVE RIBONUCLEIC-ACID FROM SOURCES ENRICHED IN RIBONUCLEASE
    CHIRGWIN, JM
    PRZYBYLA, AE
    MACDONALD, RJ
    RUTTER, WJ
    [J]. BIOCHEMISTRY, 1979, 18 (24) : 5294 - 5299
  • [5] GENOMIC SEQUENCING
    CHURCH, GM
    GILBERT, W
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1984, 81 (07): : 1991 - 1995
  • [6] Liver failure and defective hepatocyte regeneration in interleukin-6-deficient mice
    Cressman, DE
    Greenbaum, LE
    DeAngelis, RA
    Ciliberto, G
    Furth, EE
    Poli, V
    Taub, R
    [J]. SCIENCE, 1996, 274 (5291) : 1379 - 1383
  • [7] PREVENTION OF CARBON TETRACHLORIDE-INDUCED RAT-LIVER INJURY BY SOLUBLE TUMOR-NECROSIS-FACTOR RECEPTOR
    CZAJA, MJ
    XU, J
    ALT, E
    [J]. GASTROENTEROLOGY, 1995, 108 (06) : 1849 - 1854
  • [8] Liver regeneration .3. Regulation of signal transduction during liver regeneration
    Diehl, AM
    Rai, RM
    [J]. FASEB JOURNAL, 1996, 10 (02) : 215 - 227
  • [9] PROLIFERATING CELL NUCLEAR ANTIGEN - A MARKER FOR HEPATOCELLULAR PROLIFERATION IN RODENTS
    ELDRIDGE, SR
    BUTTERWORTH, BE
    GOLDSWORTHY, TL
    [J]. ENVIRONMENTAL HEALTH PERSPECTIVES, 1993, 101 : 211 - 218
  • [10] Liver regeneration .2. Role of growth factors and cytokines in hepatic regeneration
    Fausto, N
    Laird, AD
    Webber, EM
    [J]. FASEB JOURNAL, 1995, 9 (15) : 1527 - 1536