Cyclin a mRNA expression during normal rat liver cell proliferation induced by partial hepatectomy or ethinylestradiol administration

1996 ◽  
Vol 88 ◽  
pp. 93-94
Author(s):  
V. Payraudeau ◽  
J. Leblay ◽  
A. Bouant ◽  
J.P. Sarsat ◽  
J. Sobczack ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mrna Expression ◽  
Partial Hepatectomy ◽  
Rat Liver ◽  
Liver Cell ◽  
Cyclin A ◽  
Normal Rat

Influence of vinyl chloride monomer (VCM) and As2O3 on rat liver cell proliferation after partial hepatectomy

1980 ◽  
Vol 97 (1) ◽  
pp. 41-50 ◽  
Author(s):  
K. Norpoth ◽  
D. Gottschalk ◽  
I. Gottschalk ◽  
U. Witting ◽  
H. Thomas ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Partial Hepatectomy ◽  
Vinyl Chloride ◽  
Rat Liver ◽  
Liver Cell ◽  
Vinyl Chloride Monomer

Cafeteria feeding induces interleukin-1β mRNA expression in rat liver and brain

1998 ◽  
Vol 274 (6) ◽  
pp. R1734-R1739 ◽  
Author(s):  
Michael K. Hansen ◽  
Ping Taishi ◽  
Zutang Chen ◽  
James M. Krueger
Keyword(s):  
Food Intake ◽  
Mrna Expression ◽  
Rat Liver ◽  
Defense Mechanisms ◽  
Inflammatory Responses ◽  
Cafeteria Diet ◽  
Interleukin 1Β ◽  
Mrna Levels ◽  
Sleep Regulation ◽  
Normal Rat

Food intake affects gut-immune function and can provide a strong intestinal antigen challenge resulting in activation of host defense mechanisms in the digestive system. Previously, we showed that feeding rats a cafeteria diet increases non-rapid eye movement sleep by a subdiaphragmatic mechanism. Food intake and sleep regulation and the immune system share the regulatory molecule interleukin-1β (IL-1β). Thus this study examined the effects of a cafeteria diet on IL-1β mRNA and IL-1 receptor accessory protein (IL-1RAP) mRNA expression in rat liver and brain. Rats were fed normal rat chow or a palatable diet consisting of bread, chocolate, and shortbread cookies (cafeteria diet). After 3 days, midway between the light period of the light-dark cycle, rats were killed by decapitation. Feeding rats a cafeteria diet resulted in increased IL-1β mRNA expression in the liver and hypothalamus compared with rats fed only the normal rat chow. In addition, cafeteria feeding decreased IL-1RAP mRNA levels in the liver and brain stem. These results indicate that feeding has direct effects on cytokine production and together with other data suggest that the increased sleep that accompanies increased feeding may be the result of increased brain IL-1β. These results further suggest that cytokine-to-brain communication may be important in normal physiological conditions, such as feeding, as well as being important during inflammatory responses.

Upregulation of Escherichia coli heat-stable enterotoxin receptor in regenerating rat liver

1994 ◽  
Vol 266 (5) ◽  
pp. G899-G906 ◽  
Author(s):  
D. W. Laney ◽  
J. A. Bezerra ◽  
J. L. Kosiba ◽  
S. J. Degen ◽  
M. B. Cohen
Keyword(s):  
Escherichia Coli ◽  
Mrna Expression ◽  
Partial Hepatectomy ◽  
Rat Liver ◽  
Acute Phase ◽  
Chloride Secretion ◽  
Hepatocyte Proliferation ◽  
Heat Stable ◽  
Hepatocyte Regeneration ◽  
Regenerating Rat Liver

Guanylate cyclase C (GC-C) is a transmembrane protein that serves as a receptor for the recently characterized endogenous ligand guanylin and for Escherichia coli heat-stable toxin (STa). Binding of either guanylin or STa to intestinal GC-C results in net chloride secretion. Although GC-C is expressed in the rat intestine throughout life, its expression in the rat liver has previously been shown to occur only during the perinatal period. As a step toward elucidating the role of this receptor in the liver, we tested the hypothesis that GC-C mRNA expression could be induced in the adult rat liver following 1) partial hepatectomy, a stimulus for hepatocyte proliferation; 2) intraperitoneal carbon tetrachloride injection, a model of hepatocyte regeneration in the presence of inflammatory changes; and 3) subcutaneous turpentine injection, which generates an acute phase response without hepatocyte proliferation. We demonstrated expression of GC-C mRNA in the regenerating rat liver following either partial hepatectomy or CCl4-induced hepatic necrosis. We have also shown that GC-C mRNA expression occurred in association with an acute phase reaction. Coordinate with the expression of GC-C mRNA, there was upregulation of radiolabeled STa binding to liver plasma membranes prepared from turpentine-treated rats. Maximal expression of GC-C occurred in preparations enriched for the canalicular domain. Although the function of GC-C in the liver is unknown, localization to the canalicular domain would be consistent with a role for GC-C in hepatic chloride secretion, especially in the perinatal liver and during hepatocyte regeneration.

Cyclin A and liver cell proliferation

1992 ◽  
Vol 76 (2) ◽  
pp. 217-217
Author(s):  
Zindy Frédérique ◽  
Lamas Eugénia ◽  
Wang Jean ◽  
Chenivesse Xavier ◽  
Henglein Berthold ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Cell ◽  
Cyclin A

IL-22-mediated liver cell regeneration is abrogated by SOCS-1/3 overexpression in vitro

2007 ◽  
Vol 292 (4) ◽  
pp. G1019-G1028 ◽  
Author(s):  
Stephan Brand ◽  
Julia Dambacher ◽  
Florian Beigel ◽  
Kathrin Zitzmann ◽  
Malte H. J. Heeg ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mrna Expression ◽  
Liver Cell ◽  
Cytokine Signaling ◽  
Cell Regeneration ◽  
Mrna Levels ◽  
Hepatic Cells ◽  
Hepatocyte Regeneration

The IL-10-like cytokine IL-22 is produced by activated T cells. In this study, we analyzed the role of this cytokine system in hepatic cells. Expression studies were performed by RT-PCR and quantitative PCR. Signal transduction was analyzed by Western blot experiments and ELISA. Cell proliferation was measured by MTS and [3H]thymidine incorporation assays. Hepatocyte regeneration was studied in in vitro restitution assays. Binding of IL-22 to its receptor complex expressed on human hepatic cells and primary human hepatocytes resulted in the activation of MAPKs, Akt, and STAT proteins. IL-22 stimulated cell proliferation and migration, which were both significantly inhibited by the phosphatidylinositol 3-kinase inhibitor wortmannin. IL-22 increased the mRNA expression of suppressor of cytokine signaling (SOCS)-3 and the proinflammatory cytokines IL-6, IL-8, and TNF-α. SOCS-1/3 overexpression abrogated IL-22-induced STAT activation and decreased IL-22-mediated liver cell regeneration. Hepatic IL-22 mRNA expression was detectable in different forms of human hepatitis, and hepatic IL-22 mRNA levels were increased in murine T cell-mediated hepatitis in vivo following cytomegalovirus infection, whereas no significant differences were seen in an in vivo model of ischemia-reperfusion injury. In conclusion, IL-22 promotes liver cell regeneration by increasing hepatic cell proliferation and hepatocyte migration through the activation of Akt and STAT signaling, which is abrogated by SOCS-1/3 overexpression.

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