Role of ERK, p38 and PI3-kinase in EGF Receptor-Mediated Mitogenic Signalling in Cultured Rat Hepatocytes: Requirement for Sustained ERK Activation

2003 ◽  
Vol 13 (4) ◽  
pp. 229-238 ◽  
Author(s):  
Hege Thoresen ◽  
Tormod Guren ◽  
Thoralf Christoffersen
Keyword(s):  
Egf Receptor ◽  
Rat Hepatocytes ◽  
Pi3 Kinase ◽  
Erk Activation ◽  
Mitogenic Signalling ◽  
Cultured Rat Hepatocytes

X-Radiation-Induced Down-Regulation of the EGF Receptor in Primary Cultured Rat Hepatocytes

2010 ◽  
Vol 173 (5) ◽  
pp. 620-628 ◽  
Author(s):  
Akiko Maruko ◽  
Yosuke Ohtake ◽  
Masasumi Kawaguchi ◽  
Tomonori Kobayashi ◽  
Taisuke Baba ◽  
...  
Keyword(s):  
Egf Receptor ◽  
Rat Hepatocytes ◽  
Down Regulation ◽  
Primary Cultured Rat Hepatocytes ◽  
Radiation Induced ◽  
Cultured Rat Hepatocytes

EGF receptor function is required in late G1 for cell cycle progression induced by bombesin and bradykinin

2001 ◽  
Vol 281 (3) ◽  
pp. C886-C898 ◽  
Author(s):  
Chintda Santiskulvong ◽  
James Sinnett-Smith ◽  
Enrique Rozengurt
Keyword(s):  
Cell Cycle ◽  
Tyrosine Kinase ◽  
Dna Synthesis ◽  
Kinase Inhibitors ◽  
Egf Receptor ◽  
3T3 Cells ◽  
Erk Activation ◽  
Egfr Tyrosine Kinase ◽  
Swiss 3T3

We examined the role of epidermal growth factor (EGF) receptor (EGFR) tyrosine kinase activation in G protein-coupled receptor (GPCR) agonist-induced mitogenesis in Swiss 3T3 and Rat-1 cells. Addition of EGFR tyrosine kinase inhibitors (e.g., tyrphostin AG-1478) abrogated bombesin-induced extracellular signal-regulated kinase (ERK) activation in Rat-1 cells but not in Swiss 3T3 cells, indicating the importance of cell context in determining the role of EGFR in ERK activation. In striking contrast, treatment with tyrphostin AG-1478 markedly (∼70%) inhibited DNA synthesis induced by bombesin in both Swiss 3T3 and Rat-1 cells. Similar inhibition of bombesin-induced DNA synthesis in Swiss 3T3 cells was obtained using four structurally different inhibitors of EGFR tyrosine kinase. Furthermore, kinetic analysis indicates that EGFR function is necessary for bombesin-induced mitogenesis in mid-late G1 in both Swiss 3T3 and Rat-1 cells. Our results indicate that EGFR kinase activity is necessary in mid-late G1 for promoting the accumulation of cyclins D1 and E and implicate EGFR function in the coupling of GPCR signaling to the activation of the cell cycle.

Inhibitory effect of colchicine and vinblastine on transport of glucagon receptors to the plasma membrane in cultured rat hepatocytes

1985 ◽  
Vol 106 (1) ◽  
pp. 125-131 ◽  
Author(s):  
J. Watanabe ◽  
S. Kanamura ◽  
K. Kanai ◽  
M. Asada-Kubota ◽  
M. Oka
Keyword(s):  
Plasma Membrane ◽  
Rat Hepatocytes ◽  
Inhibitory Effect ◽  
Scatchard Analysis ◽  
Glucagon Receptor ◽  
Cultured Rat Hepatocytes ◽  
Glucagon Receptors

ABSTRACT The role of microtubules in the regulation of glucagon receptors on cultured rat hepatocytes was studied. Antimicrotubular reagents, colchicine and vinblastine, did not affect the binding of 125I-labelled glucagon to hepatocytes at 4°C. At 20 and 37 °C, however, the reagents reduced the binding after 60 or 90 min of incubation. Scatchard analysis indicated that the reduction in the binding was due to loss of glucagon-receptor populations. If hepatocytes were preincubated with both unlabelled glucagon and the reagents at 37 °C, the binding of the ligand to the cells decreased markedly after a certain delay. The reagents did not inhibit the internalization of the ligand in the cells until 30 min of incubation at 37 °C. The results suggest that the microtubule system plays a role in the transport of glucagon receptors to the plasma membrane, which is followed by their internalization. J. Endocr. (1985) 106, 125–131

Role of Glycosylation in Trafficking of Mrp2 in Sandwich-Cultured Rat Hepatocytes

2005 ◽  
Vol 67 (4) ◽  
pp. 1334-1341 ◽  
Author(s):  
Peijin Zhang ◽  
Xianbin Tian ◽  
Priyamvada Chandra ◽  
Kim L. R. Brouwer
Keyword(s):  
Rat Hepatocytes ◽  
Cultured Rat Hepatocytes

Hepatoprotective role of captopril on paraquat induced hepatotoxicity

2007 ◽  
Vol 26 (10) ◽  
pp. 789-794 ◽  
Author(s):  
A. Elmi ◽  
Zh Sadeghi ◽  
S. Elmi ◽  
B. Daraei ◽  
M. Ghazi-Khansari
Keyword(s):  
Cell Viability ◽  
Enzyme Inhibitor ◽  
Thiobarbituric Acid ◽  
Rat Hepatocytes ◽  
Glutathione Level ◽  
Male Wistar Rats ◽  
Cultured Rat Hepatocytes ◽  
Collagenase Perfusion ◽  
Tbars Formation

Paraquat (PQ) is a highly toxic herbicide that is used in most of the countries without restriction. The cytotoxic effect of PQ is mediated by radicals, which are the products of PQ reduction in cells. The anti-oxidative action of captopril, an angiotensin-converting enzyme inhibitor, appears to be through its ability to scavenge reactive oxygen species. In this study, the heptoprotective effect of captopril against PQ-induced hepatotoxicity was evaluated using primary cultured rat hepatocytes. Hepatocytes were isolated from male Wistar rats using a two-step collagenase perfusion, following incubation in the presence of captopril at 0.1, 0.2, 0.4 and 0.8 mM with or without PQ (5 mM). Hepatoprotective effects of captopril were studied indicating glutathione level intensity, thiobarbituric acid reactive substances (TBARs) formation, lactate dehydrogenase (LDH) leakage and cell viability every 70 min for 210 min. Captopril at 0.2 mM concentration maintained the LDH leakage, glutathione level and cell viability in the presence of 5 mM PQ. In spite of a significant elevation in TBARs formation in the PQ group, captopril did not show any significant protection. In conclusion, our data reveals that incubation of freshly isolated rat hepa-tocytes with captopril (0.2 mM) significantly protected the hepatocytes against the cytotoxicity of PQ ( P < 0.05). Human & Experimental Toxicology (2007) 26, 789— 794

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