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PubMed1990

Effect of gastrin on liver regeneration after partial hepatectomy in rats.

Gastrin has been shown to be an important trophic hormone for the mucosa of the stomach and the proximal intestine. In the present study the effect of gastrin on liver regeneration after partial hepatectomy in rats was investigated. After partial hepatectomy a significant rise in the concentration of gastrin in portal venous blood was found six, 12, and 18 hours after 70% hepatectomy. The effect of changes in the endogenous gastrin concentration on the liver regeneration was investigated in rats subjected to antrectomy or to fundectomy. Partial hepatectomy was done three weeks after the primary surgery. We found antrectomy to decrease liver regeneration, whereas fundectomy had no effect. Administration of pentagastrin 300 micrograms/kg sc three times daily for two and four days after partial hepatectomy significantly increased the rate of liver regeneration compared with controls. This study suggests that gastrin has a hepatotrophic effect. Whether this effect is caused by a direct action of gastrin on the hepatocytes or it is an indirect effect mediated by for instance insulin, glucagon or epidermal growth factor has to be further investigated.

Animals↗
PubMed1996

[Control of growth and expression of protooncogenes in regenerating liver].

There are many humoral factors involved in the control of growth in regenerating liver. The complete hepatocyte mitogens such as hepatocyte growth factor (HGF), hepatic stimulator substance (HSS) can strongly stimulate hepatocyte DNA synthesis and mitosis. The hepatocyte growth inhibitors such as transforming growth factor beta 1 (TGF beta 1), however, do not stimulate DNA synthesis, but inhibit EGF mitogenesis. In addition, the comitogens such as norepinephrine and insulin are necessary to regulate the growth of regenerating liver. It has become clear that the hepatocyte proliferation and protooncogenes are linked closely. Some protooncogenes can express specifically as markers in the different phases of the cell cycle and in hepatocytes that enter the cell cycle (G0 to G1 transit) and continue to progress.

Animals↗
PubMed2002

Inhibition of urokinase-type plasminogen activator delays expression of c-jun, activated transforming growth factor beta 1, and matrix metalloproteinase 2 during post-hepatectomy liver regeneration in mice.

BACKGROUND/AIMS: Although urokinase-type plasminogen activator (u-PA) is suggested to initiate various factors in liver regeneration after hepatectomy, no corroborative evidence has been reported. In the present study, we investigated the effect of u-PA on liver regeneration after hepatectomy. METHODS: Mice were placed into either a control group or a u-PA-inhibited group that received an in vivo u-PA inhibitor, p-aminobenzamidine. After we had removed two-thirds of the liver, we examined the expressions of c-jun mRNA and activated transforming growth factor beta 1 (TGF-beta 1), matrix metalloproteinase-2 (MMP-2) activity, and the level of hepatocyte and non-parenchymal cell proliferation in the two groups. RESULTS: In the u-PA-inhibited group, the delays in c-jun mRNA expression, hepatocyte proliferation, activated TGF-1 expression, and expression of MMP-2 activity, were 2h, 1, 2, and 1 day, respectively, and the sinusoid architecture was not restored by 10 days after hepatectomy. CONCLUSIONS: u-PA inhibition delays the expression of c-jun mRNA, hepatocyte proliferation, and restoration of the sinusoid architecture, suggesting that u-PA plays important roles in liver regeneration after hepatectomy through control of a transcription factor, c-jun expression.

Animals↗
PubMed1992

Transcriptional and posttranscriptional regulation of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase during liver regeneration.

The control of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFK-2/FBPase-2; EC 2.7.1.105/3.1.3.46) gene expression during liver regeneration was studied. The level of PFK-2/FBPase-2 mRNA decreased to about 5% of the control value 6 hr after partial hepatectomy. Thereafter the mRNA increased to a maximum at 48 hr and returned to normal levels by 96 hr. In sham-operated animals, only a small increase was observed during the first 4 hr. The mRNA was recognized by a 299-base-pair liver-specific cDNA probe but not by a muscle-specific probe. The time course of mRNA modulation was well correlated with PFK-2/FBPase-2 activity and with the amount of bifunctional enzyme protein determined by immunoblotting with an antibody raised against the N-terminal decapeptide of liver PFK-2/FBPase-2. No alteration in the degradation rate of PFK-2/FBPase-2 mRNA was noted after partial hepatectomy. The modulation of PFK-2/FBPase-2 gene expression during liver regeneration involved changes in the transcription rate. The rate decreased by 50% at 6 hr after liver resection. The rate increased thereafter to a maximum at 72 hr and then returned to control values by 96 hr. The transcription rate of albumin did not change, whereas that of phosphoenolpyruvate carboxykinase increased 12-fold at 6 hr. These results show that PFK-2/FBPase-2 gene transcription is specifically regulated and that this regulation is in part responsible for the alterations in hepatic metabolism seen in regenerating liver.

Animals↗
PubMed1987

Role of cell-surface modulator of DNA synthesis in liver regeneration.

A cell-surface modulator of DNA synthesis by cultured rat hepatocytes was studied in relation to the liver regeneration process. When rat hepatocytes isolated 24 h after partial hepatectomy were cultured, the first burst of DNA synthesis peaked at 5-8 h and declined until 24 h, followed by the second burst. Rat liver plasma membranes added 2 h after plating inhibited only the second burst, while in the case of the normal hepatocytes where the DNA synthesis began to increase after 5 h, this inhibition was observed at 16 h but not at 8 h. The inhibition did not differ when the membranes obtained from regenerating livers 12 h after partial hepatectomy were used. Epidermal growth factor binding to the cultured hepatocytes was not hindered by the membranes. These results suggest that the modulator inhibits hepatocyte proliferation at the early G1-phase of the cell cycle and that its action might be controlled by other factors in the process of liver regeneration.

Animals↗
PubMed2005

MORT1/FADD is involved in liver regeneration.

AIM: To explore the role of the adaptor molecule in liver regeneration after partial hepatectomy (PH). METHODS: We used transgenic mice expressing an N-terminal truncated form of MORT1/FADD under the control of the albumin promoter. As previously shown, this transgenic protein abrogated CD95- and CD120a-mediated apoptosis in the liver. Cyclin A expression was detected using Western blotting. ELISA and RT-PCR were used to detect IL-6 and IL-6 mRNA, respectively. DNA synthesis in liver tissue was measured by BrdU staining. RESULTS: Resection of 70% of the liver was followed by a reduced early regenerative response in the transgenic group at 36 h. Accordingly, 36 h after hepatectomy, cyclin A expression was only detectable in wild-type animals. Consequently, the onset of liver mass restoration was retarded as measured by MRI volumetry and mortality was significantly higher in the transgenic group. CONCLUSION: Our data demonstrate for the first time an involvement of the death receptor molecule MORT1/FADD in liver regeneration, beyond its well described role as part of the intracellular death signaling pathway.

Adaptor Proteins, Signal Transducing↗
PubMed1980

Enzyme activities in regenerating liver of rats.

the activities of eight enzymes were determined in the regenerating liver of rats after partial hepatectomy. For five enzymes, i.e., aldolase, lactate dehydrogenase, alanine transaminase, 5-nucleotidase, and acid phosphatase a progressive statistically significant increase in activities was obtained on days 10 and 20 of regeneration. This increase was not at the high level observed for parallel activities in fetal liver of rats on the 20th day of gestation. A possible interpretation of the process of liver regeneration is suggested.

Animals↗
PubMed1993

The coupling between transforming growth factor-alpha and the epidermal growth factor receptor during rat liver regeneration.

Transcriptional and post-transcriptional regulation of hepatic expression of the epidermal growth factor receptor (EGF-R) and its autocrine ligand, transforming growth factor-alpha (TGF-alpha), were analyzed during liver regeneration. The EGF-R mRNA levels were about twofold induced at 3 h after hepatectomy, caused by transcriptional activation. This was immediately followed by a decrease, reaching a low at half the initial level after 18 h, due to a decreased transcriptional rate. TGF-alpha mRNA expression was detected in normal liver using solution hybridization analysis. Concurrent with the decrease in EGF receptors, an increase of the TGF-alpha mRNA level occurred, starting at 6 h after hepatectomy and peaking at twice the initial TGF-alpha mRNA level after 12-24 h. For TGF-alpha, however, no increase in the rate of gene transcription could be detected. TGF-alpha and EGF competed for binding to the same hepatic receptor in normal as well as in regenerating liver. TGF-alpha bound to a similar number of binding sites as EGF in both control and 18-h posthepatectomy livers, but with 4-5 times lower affinity than EGF. At 18 h posthepatectomy, the number of binding sites was reduced to about 55% for both ligands. When the subcellular distribution of endocytosed 125I-labeled TGF-alpha was compared with that of 125I-labeled EGF, no differences were observed, and furthermore, no changes were observed in the subcellular distribution of 125I-labeled TGF-alpha during liver regeneration. The distinct and coordinate regulation of the two interactors, EGF-R and TGF-alpha, suggests that the EGF-receptor system may be functionally involved in the different phases of the prereplicative growth stimulatory process during liver regeneration.

Animals↗
PubMed1979

[Gylcine-14C incorporation into the plasma membrane proteins of normal and regenerating liver].

Incorporation of 14C-glycine in plasmatic membrane proteins of the intact and regenerating liver was studied at the beginning of G1 period of the cell cycle. The electrophoretic study of 0.05 M Na2CO3 soluble plasmatic membrane proteins of the regenerating liver showed that maximal incorporation of 14C-glycine was associated with the proteins having molecular weight of about 60 000. The pattern of incorporation of 14C-glycine in different fractions of 0.05 M Na2CO3 insoluble proteins of the plasmatic membranes of the intact and regenrating liver did not differ essentially.

Animals↗
PubMed1988

[Experimental study on lipid metabolism after partial hepatectomy--with reference to mitochondrial function of the regenerating liver].

Lipid metabolism after hepatectomy was studied in normal rats and cirrhotic rats induced with injections of thioacetamide. In normal rats, the fat accumulation in regenerating livers was observed, which had a maximal peak at 24 hours after hepatectomy. It could be a result of mobilization of fatty acids from fat tissue accompanied with hyperglucagonemia after hepatectomy. Mitochondrial respiration in regenerating liver increased remarkably. Especially when palmitoylcarnitine was used as a substrate, both the respiratory index and ATP synthesis were high until 72 hours after hepatectomy. Mitochondrial carnitine palmitoyltransferase activity was also high. The increase of mitochondrial respiration with palmitoylcarnitine as a substrate was also observed in cirrhotic liver until 72 hours after hepatectomy. These results suggest that mobilization of fatty acids increases after hepatectomy and regenerating liver utilizes fatty acids as a main substrate for hepatic regeneration.

Animals↗
PubMed1992

Fractal geometry of mosaic pattern demonstrates liver regeneration is a self-similar process.

Partial hepatectomy causes compensatory, nonneoplastic growth and regeneration in mammalian liver. Compensatory liver growth can be used to examine aspects of patterns of cell division in regenerating tissue. Chimeric animals provide markers of cell lineage which are independent of growth and can be used to follow cell division patterns. Previous experimental evidence suggests that compensatory liver growth is uniform, without focal centers of proliferation. In this study we have extended that observation to include genes important in regeneration and cell cycle control in order to establish that nascent growth centers are not present in regenerating liver. There is a uniform spatial distribution of expression of these genes which is not related to mosaic pattern in the chimeras. While these genes may help regulate hepatocyte proliferation they do not appear to regulate patch pattern in the chimeras. With this information confirming uniform growth it was possible to use fractal analysis to test various hypothesized patterns of regenerative growth in the liver. The results of this analysis indicate that mosaic pattern does not change substantially during the regenerative process. Patch area and perimeter (the area occupied by or perimeter around cells of like lineage) increase during compensatory liver growth in chimeric rats without alteration of the geometric complexity of patch boundaries (boundaries around cells of like lineage). These tissue findings are consistent with previously reported computer models of growth in which repetitive application of simple decisions assuming uniform growth created complex mosaic patterns. They support the notion that an iterating (repeating), self-similar (a pattern in which parts are representative of, but not identical to the whole) cell division program is sufficient for the regeneration of liver tissue following partial hepatectomy. Iterating, self-similar cell division programs are important because they suggest a way in which complex patterns (or morphogenesis) can be efficiently created from a small amount of stored information.

Animals↗
PubMed1995

The effect of the pineal gland on liver regeneration in rats.

BACKGROUND/AIMS: We investigated the influence of pinealectomy on liver regeneration after partial hepatectomy in rats. METHODS: Thirty rats were allocated into four groups as follows: group 1 in which no operation was done (control), group 2 in which only midline scalp incision and craniotomy was performed (sham operation), group 3 in which pinealectomy was performed and group 4 in which the rats underwent pinealectomy and pineal transplantation. Eight weeks later all the rats underwent 70% hepatectomy. RESULTS: Hepatic regenerative capacity was observed 24 h after PH by bromodeoxyuridine incorporation into DNA and the mitotic index of hepatocytes. The bromodeoxyuridine labeling indices were 45.4, 35.8, 19.9 and 36.8 in groups 1, 2, 3 and 4, respectively. The mitotic indices of the same groups were 31.2, 28.7, 8.3 and 13.4, respectively. Both the bromodeoxyuridine labeling and mitotic indices were significantly lower in the pinealectomized rats than in the control and sham operation groups. CONCLUSIONS: These results suggest that the pineal gland stimulates liver regeneration after partial hepatectomy in rats.

Animals↗