Messenger RNA expression of albumin, transferrin, transthyretin, asialoglycoprotein receptor, P450 isoform, uptake transporter and efflux transporter genes as a function of culture duration in prolonged cultured cryopreserved human hepatocytes from 7 donors as collagen-matrigel sandwich cultures: Evidence for redifferentiation upon prolonged culturing

2021 ◽  
pp. DMD-AR-2021-000424
Author(s):  
Qian Yang ◽  
Albert P. Li
1995 ◽  
Vol 182 (5) ◽  
pp. 1223-1230 ◽  
Author(s):  
P R Galle ◽  
W J Hofmann ◽  
H Walczak ◽  
H Schaller ◽  
G Otto ◽  
...  

Apoptosis occurs in the normal liver and in various forms of liver disease. The CD95 (APO-1/Fas) (CD95) receptor mediates apoptosis, and liver cells in animal models are acutely sensitive to apoptosis initiated by this receptor. We have used primary human hepatocytes as a model system to investigate CD95-mediated apoptotic liver damage. Treatment of fresh human hepatocytes with low concentrations of agonistic antibodies against CD95 resulted in apoptosis of > 95% of the cultured liver cells within 4 and 7.5 h. Immunohistology of a panel of explanted liver tissues revealed that hepatocytes in normal livers (n = 5) and in alcoholic cirrhosis (n = 13) expressed low constitutive levels of CD95. CD95 receptor expression was highly elevated in hepatocytes in hepatitis B virus-related cirrhosis (n = 9) and in acute liver failure (n = 8). By in situ hybridization CD95 ligand messenger RNA expression was absent in normal liver but detected at high levels in livers with ongoing liver damage. In cases of hepatitis B virus-related cirrhosis and acute hepatic failure, ligand expression was found primarily in areas with lymphocytic infiltration. In contrast, in patients with alcoholic liver damage, high CD95 ligand messenger RNA expression was found in hepatocytes. These findings suggest that liver destruction in hepatitis B may primarily involve killing of hepatocytes by T lymphocytes using the CD95 receptor-ligand system. In alcoholic liver damage, death of hepatocytes might occur by fratricide and paracrine or autocrine mechanisms mediated by the hepatocytes themselves.


2014 ◽  
Vol 7 (2) ◽  
pp. 117-125 ◽  
Author(s):  
Qing Zhu ◽  
Haiyan Xia ◽  
Cindy Xia ◽  
Qian Yang ◽  
Utkarsh Doshi ◽  
...  

Cancer ◽  
2011 ◽  
Vol 117 (20) ◽  
pp. 4696-4706 ◽  
Author(s):  
Violaine Havelange ◽  
Nicole Stauffer ◽  
Catherine C. E. Heaphy ◽  
Stefano Volinia ◽  
Michael Andreeff ◽  
...  

2015 ◽  
Vol 28 (6) ◽  
pp. 339-342 ◽  
Author(s):  
Ana Katherine Gonçalves ◽  
Paulo César Giraldo ◽  
Paula Renata Lima Machado ◽  
Kleber Juvenal Silva Farias ◽  
Ana Paula Ferreira Costa ◽  
...  

2006 ◽  
Vol 12 (20) ◽  
pp. 5972-5977 ◽  
Author(s):  
Tetsuro Setoyama ◽  
Shoji Natsugoe ◽  
Hiroshi Okumura ◽  
Masataka Matsumoto ◽  
Yasuto Uchikado ◽  
...  

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770163 ◽  
Author(s):  
Snigdha Saikia ◽  
Asad Ur Rehman ◽  
Prajjalendra Barooah ◽  
Preeti Sarmah ◽  
Mallika Bhattacharyya ◽  
...  

Promoter methylation reflects in the inactivation of different genes like O6-methylguanine-DNA methyltransferase DNA repair gene and runt-related transcription factor 3, a known tumor suppressor gene in various cancers such as esophageal cancer. The promoter methylation was evaluated for O6-methylguanine-DNA methyltransferase and runt-related transcription factor 3 in CpG, CHH, and CHG context (where H is A, T, or C) by next-generation sequencing. The methylation status was correlated with quantitative messenger RNA expression. In addition, messenger RNA expression was correlated with different risk factors like tobacco, alcohol, betel nut consumption, and smoking habit. CpG methylation of O6-methylguanine-DNA methyltransferase promoter had a positive association in the development of esophageal cancer (p < 0.05), whereas runt-related transcription factor 3 promoter methylation showed no significant association (p = 1.0) to develop esophageal cancer. However, the non-CpG methylation, CHH, and CHG were significantly correlated with O6-methylguanine-DNA methyltransferase (p < 0.05) and runt-related transcription factor 3 (p < 0.05) promoters in the development of esophageal cancer. The number of cytosine converted to thymine (C→T) in O6-methylguanine-DNA methyltransferase promoter showed a significant correlation between cases and controls (p < 0.05), but in runt-related transcription factor 3 no such significant correlation was observed. Besides, messenger RNA expression was found to be significantly correlated with promoter hypermethylation of O6-methylguanine-DNA methyltransferase and runt-related transcription factor 3 in the context of CHG and CHH (p < 0.05). The CpG hypermethylation in O6-methylguanine-DNA methyltransferase showed positive (p < 0.05) association, whereas in runt-related transcription factor 3, it showed contrasting negative association (p = 0.23) with their messenger RNA expression. Tobacco, betel nut consumption, and smoking habits were associated with altered messenger RNA expression of O6-methylguanine-DNA methyltransferase (p < 0.05) and betel nut consumption and smoking habits were associated with runt-related transcription factor 3 (p < 0.05). There was no significant association between messenger RNA expression of O6-methylguanine-DNA methyltransferase and runt-related transcription factor 3 with alcohol consumption (p = 0.32 and p = 0.15). In conclusion, our results suggest that an aberrant messenger RNA expression may be the outcome of CpG, CHG, and CHH methylation in O6-methylguanine-DNA methyltransferase, whereas outcome of CHG and CHH methylation in runt-related transcription factor 3 promoters along with risk factors such as consumption of tobacco, betel nut, and smoking habits in esophageal cancer from Northeast India.


1993 ◽  
Vol 66 (1) ◽  
pp. 33-42 ◽  
Author(s):  
Tsukasa Nakamura ◽  
Isao Ebihara ◽  
Mitsumine Fukui ◽  
Shiori Osada ◽  
Isao Nagaoka ◽  
...  

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