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Results for “LIVER REGENERATION”

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PubMed1992

Antibodies to tumor necrosis factor-alpha inhibit liver regeneration after partial hepatectomy.

Certain cytokines that are produced in liver may act as growth factors to facilitate wound healing and, hence, may influence liver regeneration. However, this hypothesis has not been directly tested. To determine whether the cytokine response evoked by partial hepatectomy (PH) modulates the process of liver regeneration, adult male rats were injected intraperitoneally with either goat polyclonal antibodies to rat tumor necrosis factor (TNF; 15 micrograms/g body wt) or an equal amount of goat anti-rat immunoglobulin G 1 h before PH. Animals were killed at 12, 24, 48, or 72 h post-PH, 1 h after injection with [3H]thymidine. Serum TNF levels were measured with the L929 cytotoxicity assay, titers of antibody to TNF were determined by enzyme-linked immunoabsorbent assay, and interleukin-6 (IL-6) concentrations were measured by B9 cell bioassay. Liver regeneration was assessed by [3H]thymidine incorporation into hepatic DNA and by immunohistochemical evidence of proliferating cell nuclear antigen (PCNA) expression. Antibodies to TNF were detected in treated rats but not in controls. Titers were highest at 12 h and progressively fell. Although TNF was never detected in serum, treatment with anti-TNF pre-PH significantly inhibited increases in serum IL-6 concentration post-PH. Anti-TNF pretreatment also inhibited [3H]thymidine incorporation into DNA, as well as expression of PCNA by both hepatocytes and liver nonparenchymal cells. These data indicate that TNF positively modulates liver regeneration after PH.

Animals↗
PubMed1991

TNF-driven inflammation during mouse liver regeneration after partial hepatectomy and its role in growth regulation of liver.

To determine the role of TNF-driven inflammation in self-regulation of cell growth and differentiation, mouse liver regeneration after partial hepatectomy was examined for TNF-driven inflammation. Hepatectomy provoked priming state for TNF production in both whole body and liver on day 3 when the peak mitotic response occurred. Histochemical studies of liver also showed an inflammatory symptom; hepatocellular necrotic foci appeared by 6 hours after hepatectomy. TNF itself was secreted spontaneously in liver transiently on day 1 to 2 after hepatectomy just before the proliferation of hepatocytes. Dexamethasone reduced both TNF secretion and hepatocyte proliferation after hepatectomy. Recombinant murine TNF stimulated the in vitro proliferation of hepatocytes. These findings indicate that hepatectomy induces short-term secretion of TNF in liver and TNF-driven inflammation has an important role in liver regeneration, at least in part by the direct stimulation of hepatocyte proliferation.

Animals↗
PubMed1998

[Characterization of liver regeneration in the albumin-urokinase transgenic mouse].

UNLABELLED: Models of liver regeneration are essential to understand mechanisms of hepatic carcinogenesis, correct genetic diseases by gene transfer or hepatocyte transplantation. The expression in the liver of transgenic mice of a gene coding for a urokinase-type plasminogen activator (uPA mouse) induces hepatotoxicity and prolonged post-native liver regeneration from cellular clones which have inactivated the transgene. This model may have major applications but it remains necessary to characterize the liver regeneration pattern. METHODS: Histological and immunohistochemical studies of the liver of uPA and non-transgenic mice, 3, 7, 14, 21, 28, 42 and 56 days-old. Markers of cellular proliferation: 5-bromo-2'deoxyuridine (BrdU) and proliferating cell nuclear antigen (PCNA). RESULTS: Regenerative nodules were seen from day 14. These nodules then grew, became confluent and by 8 weeks constituted the entire liver mass. A semi-quantitative study of BrdU and PCNA showed a maximal labeling at day 7 (300 to 350 labeled cells/10 microscopic fields, mag 400). When the nodules appeared, 60 to 80% of the cells were labeled. The proportion of labeled cells decreased but was still greater than that observed in non transgenic mice up to day 56 (92 to 106 labeled cells vs 10 to 28, on day 28). CONCLUSIONS: In uPA mouse liver regeneration is significantly expanded, as compared to the regeneration following partial hepatectom. This study therefore has allowed to determine the best conditions for using this model.

Animals↗
PubMed1997

Nuclear ADP-ribosylation factor (ARF)- and oleate-dependent phospholipase D (PLD) in rat liver cells. Increases of ARF-dependent PLD activity in regenerating liver cells.

Two forms of phospholipase D (PLD) have been found to be present in nuclei isolated from rat hepatocytes by measuring phosphatidylbutanol produced from exogenous radiolabeled phosphatidylcholine in the presence of butanol. In nuclear lysates from either rat liver or ascites hepatoma AH 7974 cells, the PLD activity was markedly stimulated by a recombinant ADP-ribosylation factor (rARF) in the presence of the guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS) and phosphatidylinositol 4, 5-bisphosphate. ATP and phorbol-12-myristate 13-acetate had no synergistic effect on this PLD activity. On the other hand, the nuclear PLD was stimulated by unsaturated fatty acids, especially by oleic acid. The ARF-dependent nuclear PLD activity was increased in the S-phase of the regenerating rat liver after partial hepatectomy and also was much higher in AH 7974 cells than in the resting rat liver. In contrast, the levels of the oleate-dependent PLD activity remained constant throughout the cell cycle in liver regeneration. The intranuclear levels of the stimulating proteins of the nuclear PLD activity, e.g. ARF, RhoA, and protein kinase Cdelta increased in the S-phase of the regenerating liver. These results suggested that the nuclear ARF-dependent PLD activity may be associated with cell proliferation.

ADP-Ribosylation Factors↗
PubMed2005

Morpholino oligonucleotide-triggered beta-catenin knockdown compromises normal liver regeneration.

BACKGROUND/AIMS: Wnt/beta-catenin activation is seen during early liver regeneration (LR) observed as stabilization and translocation to the nucleus followed by an overall decrease. However, beta-catenin continues to be in hepatocyte nucleus and membrane, secondary to its increased gene expression at 6-72 h. METHODS: In the present study, we examined the effect of ablating beta-catenin transcription on LR. Twelve male fisher rats were subjected to two-third partial hepatectomy followed by administration of beta-catenin antisense phospho-morpholino oligonucleotide (AS) in six or mismatch control (CON) injection in the remaining 6 via superior mesenteric vein. Three animals from each group were sacrificed at 24 h and 7 days for liver assessment. RESULTS: AS group exhibited a significant decrease in total beta-catenin at 24 h. A significant decrease in liver/body weight ratio was also observed in the AS group at 24 h and 7 days that was due to decreased proliferation. Among the targets of this pathway c-myc and uPAR levels showed significant decrease while cyclin-D1 remained unaffected. CONCLUSIONS: We demonstrate the importance of beta-catenin in early liver regeneration especially in hepatocyte proliferation. Also, c-myc and uPAR might be crucial downstream effectors of beta-catenin during liver regeneration.

Animals↗
PubMed1989

High density lipoproteins during rat liver regeneration.

Compositional and maturative parameters of high density lipoproteins (HDL) have been examined during the early stages of rat liver regeneration, when lecithin:cholesterol acyltransferase (LCAT) activity, responsible for the maturation of this lipoprotein class, is markedly decreased. Both HDL subclass distribution and chemical composition are not significantly different from the control, except for a slightly lower cholesterol ester content. Few disc-shaped particles are detectable by electron microscopic observation. Cholesterol ester decrease and presence of immature particles are related, but the entity of the modification is lower than suggested by the deep decrease of LCAT activity. This seems to indicate that proper HDL maturation is assured in the regenerating liver despite low LCAT activity.

Animals↗
PubMed1975

The effect of alpha-melanophor-stimulating hormone on liver regeneration and incorporation of amino acid in rats' liver protein.

Following 25 mug/day synthetic alpha-MSH administration, the liver regeneration of partially hepatectomized rats proved to be increased. The hormone treatment resulted in an enhanced alanine incorporation of the liver proteins, but this effect was uncertain on partially hepatectomized rats. Due to the hormone treatment the low liver protein content of the operated rats became normal. The pseudocholinesterase activity of the liver homogenate of alpha-MSH treated rats was also elevated. On the basis of these experiments authors are supposing some protein synthesis increasing effect of synthetic alpha-MSH.

Alanine↗