scholarly journals Suppression of liver cell apoptosis in vitro by the non-genotoxic hepatocarcinogen and peroxisome proliferator nafenopin.

1994 ◽  
Vol 125 (1) ◽  
pp. 197-203 ◽  
Author(s):  
A C Bayly ◽  
R A Roberts ◽  
C Dive
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Liver Cell ◽  
Hepatoma Cell ◽  
Chromatin Condensation ◽  
Hepatoma Cell Line ◽  
Peroxisome Proliferator ◽  
Tgf Beta ◽  
Induced Apoptosis ◽  
Co Addition

Suppression of apoptosis has been implicated as a mechanism for the hepatocarcinogenicity of the peroxisome proliferator class of non-genotoxic carcinogens. The ability of the peroxisome proliferator nafenopin to suppress or delay the onset of liver apoptosis was investigated using primary cultures of rat hepatocytes and the Reuber hepatoma cell line FaO. 50 microM nafenopin reversibly maintained the viability of primary rat hepatocyte cultures which otherwise degenerated within 8 d of establishment. The maintenance of viability of hepatocyte monolayers was associated with a significant decrease in the number of cells exhibiting chromatin condensation patterns typical of apoptosis. Apoptosis could be induced in hepatocytes by administration of 5 ng/ml TGF beta 1. Co-addition of 50 microM nafenopin significantly reduced TGF beta 1-induced apoptosis by 50-60%. TGF beta 1 (1-5 ng/ml) also induced apoptosis in the FaO rat hepatoma cell line. Cell death was accompanied by detachment of FaO cells from the monolayer and detached cells exhibited chromatin condensation and non-random DNA fragmentation patterns typical of apoptosis. Co-addition of 50 microM nafenopin to TGF beta 1-treated FaO cultures significantly reduced the number of apoptotic cells detaching from the monolayer at 24 h. In contrast, nafenopin had no significant effect on FaO apoptosis induced by the DNA damaging agents etoposide and hydroxyurea. We conclude that suppression of liver cell death by apoptosis may play a role in the hepatocarcinogenicity of the peroxisome proliferators, although the extent of this protection is dependent on the nature of the apoptotic stimulus.

Non-genotoxic hepatocarcinogenesis in vitro: the FaO hepatoma line responds to peroxisome proliferators and retains the ability to undergo apoptosis

1993 ◽  
Vol 104 (2) ◽  
pp. 307-315 ◽  
Author(s):  
A.C. Bayly ◽  
N.J. French ◽  
C. Dive ◽  
R.A. Roberts
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Cell Lines ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferators ◽  
Hepatoma Cell Lines

A range of hepatoma cell lines (RH1, HTC, FaO, 7800C1 and MH1C1), has been studied with the aim of establishing an in vitro model to investigate the molecular mechanisms of hepatocarcinogenicity induced by the peroxisome proliferator class of non-genotoxic carcinogens. In view of speculation that peroxisome proliferators suppress hepatocyte apoptosis in vivo, we have placed particular emphasis on evaluating whether hepatoma cell lines retain the ability to undergo apoptotic cell death. Expression of the liver-specific differentiation marker albumin and the peroxisome proliferator-activated receptor (PPAR) was highest in the Reuber hepatoma cell line, FaO. This cell line also demonstrated the most marked response to the peroxisome proliferator nafenopin with a 2.2-fold induction of the microsomal enzyme cytochrome p450IVA1. This response was found to display intercellular heterogeneity by immunocytochemistry. Thus, the FaO cell line maintained characteristics of hepatocytes, both in vivo and in vitro, in terms of expression of constitutive and inducible markers. However, none of the cell lines tested mirrored the hyperplastic response of hepatocytes to nafenopin, since no increase in cell growth kinetics was observed on addition of nafenopin to the growth medium. The mode of cell death in confluent FaO cultures was characterised as apoptosis, by fluorescence microscopy and agarose gel electrophoresis of extracted DNA. Cells detaching from confluent FaO cultures exhibited chromatin condensation and DNA fragmentation patterns characteristic of cels undergoing apoptotic death.Interestingly, no apoptosis was seen in monolayer cells, suggesting that apoptosis in vitro is associated with cell shrinkage and detachment similar to that documented for the liver in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Evidence for trans regulation of apoptosis in intertypic somatic cell hybrids.

1994 ◽  
Vol 14 (9) ◽  
pp. 6125-6134 ◽  
Author(s):  
H Gourdeau ◽  
P R Walker
Keyword(s):  
Cell Death ◽  
Somatic Cell ◽  
Cell Line ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Suspension Cells ◽  
Glucocorticoid Treatment ◽  
Cell Hybrids ◽  
Genetic Components ◽  
Cell Death Pathway

The genetic components required for glucocorticoid induction of apoptosis were studied by using somatic cell hybridization. Intertypic whole-cell hybrids were generated by crossing the glucocorticoid-resistant rat liver cell line Fado-2 with the glucocorticoid-sensitive mouse thymoma cell line BW5147.3. Morphological and biochemical criteria were used to assess sensitivity or resistance to glucocorticoid-induced cell death. Both phenotypes were observed, and all of the hybrids retained a functional glucocorticoid receptor as judged by their abilities to induce the metallothionein gene in response to dexamethasone (Dex). Sensitivity to apoptosis did not correlate with morphological phenotype in that not all suspension cells were sensitive. The effect of glucocorticoids on the expression of apoptosis-linked genes was analyzed in a subset of Dex-sensitive and Dex-resistant hybrids. p53 and c-myc mRNAs were present in parental cells as well as sensitive and resistant hybrid cells, and their levels were not affected by glucocorticoid treatment. bcl-2 expression was restricted to the thymoma cell line and was also not affected by glucocorticoids. We did not detect any bcl-2 mRNA in the hepatoma cell line and the hybrids, suggesting that, as with most tissue-specific genes, bcl-2 is regulated in trans. Furthermore, while the majority of hybrids analyzed retained a full complement of mouse chromosomes, sensitive hybrids were missing some rat chromosomes (preferentially chromosomes 16 and 19), indicating that apoptosis is subject to trans repression. Resistant cells thus appear to repress the activity or synthesis of a nuclear factor that interacts with a glucocorticoid-dependent gene(s) to activate the cell death pathway.

Caudatin-2,6-dideoxy-3-O-methy-β-d-cymaropyranoside 1 induced apoptosis through caspase 3-dependent pathway in human hepatoma cell line SMMC7721

2010 ◽  
Vol 25 (5) ◽  
pp. 631-637 ◽  
Author(s):  
Yun-ru Peng ◽  
Yong-fang Ding ◽  
Ying-jie Wei ◽  
Bin Shu ◽  
You-bin Li ◽  
...  
Keyword(s):  
Cell Line ◽  
Caspase 3 ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Human Hepatoma Cell Line ◽  
Induced Apoptosis ◽  
Dependent Pathway

Dexamethasone enhances trichosanthin-induced apoptosis in the HepG2 hepatoma cell line

Life Sciences ◽  
2010 ◽  
Vol 86 (1-2) ◽  
pp. 10-16 ◽  
Author(s):  
Meng Li ◽  
Fei Chen ◽  
Cui-Ping Liu ◽  
Dong-Mei Li ◽  
Xiang Li ◽  
...  
Keyword(s):  
Cell Line ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Induced Apoptosis ◽  
Hepg2 Hepatoma Cell

scholarly journals Role of MAP kinases and their cross-talk in TGF-β1-induced apoptosis in FaO rat hepatoma cell line

Hepatology ◽  
2002 ◽  
Vol 35 (6) ◽  
pp. 1360-1371 ◽  
Author(s):  
Hyun-Jin Park ◽  
Byung-Chul Kim ◽  
Seong-Jin Kim ◽  
Kyeong Sook Choi
Keyword(s):  
Cell Line ◽  
Cross Talk ◽  
Map Kinases ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Induced Apoptosis ◽  
Rat Hepatoma Cell Line ◽  
Tgf Β1 ◽  
Rat Hepatoma
Sign in / Sign up

Export Citation Format

Share Document