Induction of c-fos gene by mercury chloride in LLC-PK1 cells

被引:15
作者
Matsuoka, M [1 ]
Wispriyono, B [1 ]
Igisu, H [1 ]
机构
[1] Univ Occupat & Environm Hlth, Dept Environm Toxicol, Yahatanishi Ku, Kitakyushu, Fukuoka 807, Japan
关键词
c-fos; c-Fos protein; mercury chloride; LLC-PK1; cells; nephrotoxicity;
D O I
10.1016/S0009-2797(97)00097-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The c-fos, a member of the immediate early genes, has been reported to be expressed in the renal proximal tubule in response to ischemic and toxic injury. In the present study, effects of mercury chloride (HgCl2) on the expression of c-fos were examined in LLC-PK1 cells. The reverse transcription polymerase chain reaction (RT-PCR) analysis for the semi-quantification of mRNA showed that the treatment of 20 mu M HgCl2 markedly increased c-fos mRNA levels. The level of c-fos mRNA began to increase after a 30-min exposure, peaked at 1 h and then returned to the control level at 8 h. The HgCl2-induced c-fos expression was abolished completely by actinomycin-D, indicating it was due to transcriptional activation of the gene. Western blotting immunodetection revealed accumulation of c-Fos protein after 1 h exposure to 20 mu M HgCl2. The cytotoxicity of HgCl2 as assayed by mitochondrial dehydrogenase activity (MTT conversion) was observed after 18 h exposure but not at 0.5-8 h. Also, the decrease in cell viability was accompanied with DNA fragmentation, which is characteristic of apoptosis. The present results showed that HgCl2 could induce the early expression of c-fos gene in a renal epithelial cell line. (C) 1997 Elsevier Science Ireland Ltd.
引用
收藏
页码:95 / 106
页数:12
相关论文
共 28 条
[1]   THE ROLE OF JUN, FOS AND THE AP-1 COMPLEX IN CELL-PROLIFERATION AND TRANSFORMATION [J].
ANGEL, P ;
KARIN, M .
BIOCHIMICA ET BIOPHYSICA ACTA, 1991, 1072 (2-3) :129-157
[2]   CASCADE INDUCTION OF C-FOS, C-MYC, AND HEAT-SHOCK 70K TRANSCRIPTS DURING REGRESSION OF THE RAT VENTRAL PROSTATE-GLAND [J].
BUTTYAN, R ;
ZAKERI, Z ;
LOCKSHIN, R ;
WOLGEMUTH, D .
MOLECULAR ENDOCRINOLOGY, 1988, 2 (07) :650-657
[3]   THYROTROPIN-RELEASING-HORMONE STIMULATES C-JUN AND C-FOS MESSENGER-RIBONUCLEIC-ACID LEVELS - IMPLICATIONS FOR CALCIUM MOBILIZATION AND PROTEIN-KINASE-C ACTIVATION [J].
CARR, FE ;
FISHER, CU ;
FEIN, HG ;
SMALLRIDGE, RC .
ENDOCRINOLOGY, 1993, 133 (04) :1700-1707
[4]  
COHEN D R, 1989, Critical Reviews in Oncogenesis, V1, P65
[5]  
DuncanAchanzar KB, 1996, J PHARMACOL EXP THER, V277, P1726
[6]  
GSTRAUNTHALER GJA, 1988, RENAL PHYSIOL BIOCH, V11, P1
[7]   Mechanisms of apoptosis and its potential role in renal tubular epithelial cell injury [J].
Lieberthal, W ;
Levine, JS .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY, 1996, 271 (03) :F477-F488
[8]   ROLE OF [CA2+]I IN INDUCTION OF C-FOS, C-JUN, AND C-MYC MESSENGER-RNA IN RAT PTE AFTER OXIDATIVE STRESS [J].
MAKI, A ;
BEREZESKY, IK ;
FARGNOLI, J ;
HOLBROOK, NJ ;
TRUMP, BF .
FASEB JOURNAL, 1992, 6 (03) :919-924
[9]  
MATSUOKA H, 1996, ENVIRON TOXICOL PHAR, V2, P373
[10]   CADMIUM-INDUCED EXPRESSION OF IMMEDIATE-EARLY GENES IN LLC-PK1 CELLS [J].
MATSUOKA, M ;
CALL, KM .
KIDNEY INTERNATIONAL, 1995, 48 (02) :383-389