Liver cell specific TGF-beta sensitivity and outcome

2018 ◽  
Vol 56 (08) ◽  
pp. e251-e251
Author(s):  
M Han ◽  
ZC Nwosu ◽  
MP Ebert ◽  
S Hammad ◽  
C Meyer ◽  
...  
Keyword(s):  
1994 ◽  
Vol 125 (1) ◽  
pp. 197-203 ◽  
Author(s):  
A C Bayly ◽  
R A Roberts ◽  
C Dive

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.


2019 ◽  
Author(s):  
M Han ◽  
ZC Nwosu ◽  
MP Ebert ◽  
S Hammad ◽  
S Dooley ◽  
...  

Author(s):  
Robert R. Cardell

Hypophysectomy of the rat renders this animal deficient in the hormones of the anterior pituitary gland, thus causing many primary and secondary hormonal effects on basic liver functions. Biochemical studies of these alterations in the rat liver cell are quite extensive; however, relatively few morphological observations on such cells have been recorded. Because the available biochemical information was derived mostly from disrupted and fractionated liver cells, it seemed desirable to examine the problem with the techniques of electron microscopy in order to see what changes are apparent in the intact liver cell after hypophysectomy. Accordingly, liver cells from rats which had been hypophysectomized 5-120 days before sacrifice were studied. Sham-operated rats served as controls and both hypophysectomized and control rats were fasted 15 hours before sacrifice.


2001 ◽  
Vol 120 (5) ◽  
pp. A495-A495
Author(s):  
Y GANG ◽  
S DANOVITCH ◽  
T FLEURY ◽  
B MISHRA ◽  
C DENG ◽  
...  

1959 ◽  
Vol 37 (6) ◽  
pp. 760-765 ◽  
Author(s):  
S.W. Berkheiser

Author(s):  
Mythreye Karthikeyan ◽  
Gerard Blobe
Keyword(s):  
Type I ◽  

2009 ◽  
Vol 47 (10) ◽  
Author(s):  
J Ellermeier ◽  
J Wie ◽  
P Düwell ◽  
S Endres ◽  
M Schnurr

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