Regeneration of Mammalian Liver

Bucher, Nancy L. R.

doi:10.1016/s0074-7696(08)61119-5

Cited by 642 publications

(221 citation statements)

References 237 publications

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“…In both of the experimental groups physiological alterations begin immediately after induction of insult. In 70% liver resection, as we and others have shown previously, 11,22,23 these changes increase with time to reach a peak at almost 24 hours and afterwards gradually return to normal, with an approximately 80% mortality rate 40 to 70 to mesenteric lymph nodes, liver, and spleen in ALI-DG (acute liver hours later. We found it reasonable to assume that at injury induced by D-galactosamine) group at 24 and 48 hours.…”

Section: Discussionsupporting

confidence: 62%

Bacterial translocation in acute liver injury induced by d- galactosamine

Kasravi

Wang

et al. 1996

Hepatology

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Acute liver injury and hepatic failure are serious Acute liver injury is associated with a high rate of infectious and septic complications. Most of these infec-clinical conditions that are sometimes observed in extions are produced by gram negative enteric bacteria. tensive hepatic surgery and in patients with multiple We evaluated bacterial translocation, intestinal perme-system organ failure. 1,2 Bacterial infection and sepsis ability, blood flow, portal pressure, and intestinal mi-are recognized as dangerous complications of this remcroflora after induction of liver injury and 70% liver re-edy with significant share in its morbidity and mortalsection in the rat. The rate of translocation to both portal ity. [3][4][5] Gram-negative enteric bacteria are frequent and arterial blood was 100% at 24 hours and 50% at 48 causative organisms in most of the published studies. 6-8 hours after liver resection compared with 83% to portal It has been shown that the gut, as a reservoir of enteric vein and 50% to aortic blood at both time points after bacteria in the body, plays an important role in many acute liver injury. Translocation to intraabdominal orcritical clinical situations, such as major burns, hemorgans (liver, spleen, and mesenteric lymph nodes) was rhagic shock, and so on. 9 Under normal conditions a 100% in both groups at both 24 and 48 hours. The rate series of protective measures, such as mucosal barrier of translocation increased after liver injury at 48 hours with progression of the liver injury but was decreased function, immunoglobulin secretion, and local and sysin the 70% liver resection group with improvement of temic macrophage system prevent translocation of liver function. ''Total aerobic'' and ''total anaerobic'' bac-these potential pathogens to the extraintestinal sites. 10 terial counts in small intestine and cecum were not af-Severe clinical disorders may disrupt these normal profected. Pulmonary, distal small intestine, and cecal tective mechanisms and make it possible for the intestiblood flow were decreased in both groups, whereas nal bacteria to translocate. Translocation of endotoxin blood flow in the proximal small intestine was unaf-and intestinal bacteria in acute liver injury may intenfected. Portal pressure and flow were increased after sify the extent of injury and may also be responsible 70% liver resection, but they were decreased in acute for the high rate of associated infection and sepsis obliver injury. After acute liver injury, permeability of both served in these patients. So far, little attention has MATERIALS AND METHODSgery, Lund University, 221 85 Lund, Sweden. Experimental Groups.One hundred eight Sprague-

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Section: Discussionsupporting

confidence: 62%

Bacterial translocation in acute liver injury induced by d- galactosamine

Kasravi

Wang

et al. 1996

Hepatology

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“…Hepatic regeneration is an important component of the recovery process that occurs after various hepatic injuries. 46 Previous studies of liver regeneration following acute liver damage or partial hepatectomy demonstrated that the hepatic biomatrix contains large amounts of HGF, 47 predominantly around portal triads. 48 Matrix breakdown may cause rapid release of HGF, thus accounting for the rapid increase in HGF levels in the blood plasma.…”

Section: Discussionmentioning

confidence: 99%

Baculovirus-mediated interferon alleviates dimethylnitrosamine-induced liver cirrhosis symptoms in a murine model

et al. 2008

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The wild-type baculovirus Autographa californica multiple nuclear polyhedrosis virus (AcMNPV) infects a range of mammalian cell types in vitro but does not replicate in these cells. The current study investigated the in vivo effect of AcMNPV in the mouse model of liver cirrhosis induced by the mutagen dimethylnitrosamine. Intraperitoneal injection of AcMNPV induced an immune response. The baculovirus was taken up by the liver and spleen where it suppressed liver injury and fibrosis through the induction of interferons. This study presents the first evidence of the feasibility of using baculovirus to treat liver cirrhosis. Gene Therapy (2008) 15, 990-997;

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“…After PH in male BALB/c mice, a large population of hepatocytes progresses through the cell cycle in a relatively synchronous manner, with peak DNA synthesis occurring 36 h after the procedure (Cornell et al, 1990;Albrecht et al, 1994). At later time points, DNA synthesis is diminished and represents asynchronous hepatocyte replication and division of nonparenchymal liver cells (Grisham, 1962;Bucher, 1963). By 120 h after the procedure, DNA synthesis returns to near-basal levels.…”

Section: Expression Of P21 and P27 Proteins During Liver Regenerationmentioning

confidence: 99%

“…There were no apparent di erences in liver weight or anatomy before PH in the two strains of mice (data not shown). The interval between PH and peak DNA synthesis in rodents is a ected by several variables, including species, strain, sex, age and diet (Michalopoulos and DeFrances, 1997;Bucher, 1963). For example, studies in female mice of other strains indicate that peak DNA synthesis occurs 48 h after PH, rather than 36 h, as seen in male BALB/c mice (Paulsen, l990;Lorup, 1977).…”

Section: Regulation Of Cdk2 Activity By P27mentioning

confidence: 99%

Involvement of p21 and p27 in the regulation of CDK activity and cell cycle progression in the regenerating liver

et al. 1998

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In tissue culture systems, p21 and p27 inhibit cyclindependent kinase (CDK) activity and cell cycle progression in response to numerous stimuli, but little is known about their involvement in cell growth in vivo. We examined the modulation of CDK activity by these proteins after 70% partial hepatectomy (PH), an in vivo model of synchronous hepatocyte cell cycle progression. After PH in BALB/c mice, p21 was induced during the prereplicative (G1) phase and was maximally expressed after peak hepatocyte DNA synthesis. p27 was present in quiescent liver and was minimally induced after PH. p21 and p27 immunoprecipitated with CDK2, CDK4, and cyclin D1 in the regenerating liver. The activity of CDK2-, CDK4-and cyclin D1-associated kinases was upregulated after PH, and maximal activity of these enzyme complexes corresponded to peak DNA synthesis. Immunodepletion experiments suggested that p27 plays a role in downregulating CDK2 activity before and after peak DNA synthesis. Compared to cogenic wild-type mice, p217/7 mice demonstrated evidence of markedly accelerated hepatocyte progression through G1 phase after PH: DNA synthesis, upregulation of cyclin A and PCNA, induction of cyclin D1-and CDK2-associated kinase activity, and appearance of a phosphorylated retinoblastoma protein (Rb) species occurred earlier in the p217/7 mice. These results suggest that p21 and p27 modulate CDK activity in the regenerating liver, and that p21 regulates the rate of progression through G1 phase of the cell cycle in vivo.

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Regeneration of Mammalian Liver

Cited by 642 publications

References 237 publications

Bacterial translocation in acute liver injury induced by d- galactosamine

Bacterial translocation in acute liver injury induced by d- galactosamine

Baculovirus-mediated interferon alleviates dimethylnitrosamine-induced liver cirrhosis symptoms in a murine model

Involvement of p21 and p27 in the regulation of CDK activity and cell cycle progression in the regenerating liver

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