The Effect of Denervation on Liver Regeneration in Partially Hepatectomized Rats

Hamada, Takayuki; Eguchi, Susumu; Yanaga, Katsuhiko; Inuo, Hiroyuki; Yamanouchi, Kaoru; Kamohara, Yukio; Okudaira, Sadayuki; Tajima, Yoshitsugu; Kanematsu, Takashi

doi:10.1016/j.jss.2007.01.007

Cited by 13 publications

(15 citation statements)

References 22 publications

(24 reference statements)

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“…In summary, this study analyzed the regulatory role of autonomic nerves during rat liver regeneration at transcription level, and found that splanchnic nerves and vagal nerves could regulate the expression of liver regenerationrelated genes and thereby affect rat liver regeneration (Hamada et al 2007). In future, western-blot, gene knockin and RNA interference are needed to further explore the regulatory roles of autonomic nervous system in vitro and in vivo during rat liver regeneration.…”

Section: Discussionmentioning

confidence: 98%

“…Tanaka et al (1987) revealed that liver vagotomy delayed the progress of rat liver regeneration (LR), but did not inhibit its DNA synthesis. Hamada et al (2007) proved that total liver denervation did not affect the growth rate of rat regenerating livers at 12-120 h after partial hepatectomy (PH), but the ratio of liver weight to body weight was significantly higher than control at 168 h after PH, and it was suggested total liver denervation could promote LR after PH. At present, it is well documented that the quiescent hepatocytes are activated in the priming phase of 0.5-4 h post PH (Guo et al 2006).…”

Section: Introductionmentioning

confidence: 99%

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Role of the Autonomic Nervous System in Rat Liver Regeneration

Zhang

Wang

et al. 2011

Cell Mol Neurobiol

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To study the regulatory role of autonomic nervous system in rat regenerating liver, surgical operations of rat partial hepatectomy (PH) and its operation control (OC), sympathectomy combining partial hepatectomy (SPH), vagotomy combining partial hepatectomy (VPH), and total liver denervation combining partial hepatectomy (TDPH) were performed, then expression profiles of regenerating livers at 2 h after operation were detected using Rat Genome 230 2.0 array. It was shown that the expressions of 97 genes in OC, 230 genes in PH, 253 genes in SPH, 187 genes in VPH, and 177 genes in TDPH were significantly changed in biology. The relevance analysis showed that in SPH, genes involved in stimulus response, immunity response, amino acids and K(+) transport, amino acid catabolism, cell adhesion, cell proliferation mediated by JAK-STAT, Ca(+), and platelet-derived growth factor receptor, cell growth and differentiation through JAK-STAT were up-regulated, while the genes involved in chromatin assembly and disassembly, and cell apoptosis mediated by MAPK were down-regulated. In VPH, the genes associated with chromosome modification-related transcription factor, oxygen transport, and cell apoptosis mediated by MAPK pathway were up-regulated, but the genes associated with amino acid catabolism, histone acetylation-related transcription factor, and cell differentiation mediated by Wnt pathway were down-regulated. In TDPH, the genes related to immunity response, growth and development of regenerating liver, cell growth by MAPK pathway were up-regulated. Our data suggested that splanchnic and vagal nerves could regulate the expressions of liver regeneration-related genes.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Role of the Autonomic Nervous System in Rat Liver Regeneration

Zhang

Wang

et al. 2011

Cell Mol Neurobiol

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“…In the liver, age-related changes have been shown to include a reduction of liver mass and the dysfunction of protein M) for 1 h. Subsequently, TG2 cross-linking activity in hepatocytes was assessed by [1,[4][5][6][7][8][9][10][11][12][13][14] C]putrescine incorporation into proteins of hepatocytes. The radioactivity of [1,4-14 C]putrescine incorporated into proteins of cells was measured using a Beckman LS 6500 liquid scintillation counter.…”

Section: Discussionmentioning

confidence: 99%

“…In the case of treatment with calcium chelator and NE, the hepatocytes were pretreated for 1 h with EGTA (2 mM) or BAPTA-AM (5 mM) before NE treatment. [1,[4][5][6][7][8][9][10][11][12][13][14] C]putrescine was added at the time of EGF treatment in cultured hepatocytes. After 1-h incubation, hepatocytes were harvested with distilled water.…”

Section: Methodsmentioning

confidence: 99%

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Effect of aging on norepinephrine-related proliferative response in primary cultured periportal and perivenous hepatocytes

Kobayashi

Saito

Ohtake

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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(NE) amplifies the mitogenic effect of EGF in a rat liver through the adrenergic receptor coupled with G protein, Gh␣. Gh␣ is also known as a transglutaminase 2 (TG2), whose cross-linking activity is implicated in hepatocyte growth. Recently, we found that NE-induced amplification of EGF-induced DNA synthesis in hepatocytes obtained from perivenous regions of liver is caused by inhibiting the downregulation of EGF receptor (EGFR) by TG2. In the present study, we investigated the effect of aging on NE-related proliferative response. Hepatocytes were obtained from the liver of 7-and 90-wk-old rats. To examine this in detail, periportal hepatocytes (PPH) and perivenous hepatocytes (PVH) were isolated using the digitonin/collagenase perfusion technique. EGF or NE receptor binding was analyzed by Scatchard analysis. Changes in NE-induced DNA synthesis, G protein activity, and TG2 activity were measured. NE slightly potentiated [ 125 I]EGF binding to EGFR, and EGF-induced DNA synthesis in PVH but not in PPH.[ 3 H]NE binding studies indicated that PVH have a greater number of receptors than PPH, and that the number of receptors in both subpopulations increased with aging. NE-induced changes in G protein activity and TG2 activity in 90-wk-old rats were slight compared with 7-wk-old rats. These results suggest that NE results in a slight recovery effect on the age-related decline in EGF-induced DNA synthesis because of incomplete switching of the function from TG2 to Gh␣. transglutaminase; EGFA SIGNIFICANT DECREASE IN cell proliferation is a hallmark of aging in many cell lines (6,14,17,34,36). A regeneration of rat liver is widely used as a model of aged cell proliferative capacity and responsiveness (5, 17). The decline of DNA synthesis and loss of regeneration capacity are a typical phenomena associated with liver senescence. It has been shown that a faulty restoration of an aged liver is caused by a delayed cell cycle and a reduction of the number of proliferating hepatocytes (5, 49). However, the mechanism by which aging causes impairment of the responsiveness of DNA synthesis to various growth factors and cytokines is still unclear. Hepatocytes are distinguished between periportal hepatocytes (PPH) and perivenous hepatocytes (PVH) on the basis of their metabolism and growth factor responsiveness (12, 32). In particular, EGF and hepatocyte growth factor (HGF) both facilitate hepatocyte proliferation. (15). Many studies have shown that EGF binds EGF receptors (EGFR) with two distinct affinities and subpopulations of EGFR (41). Macdonald and Pike (24) recently provided the evidence that affinities of EGF binding to EGFR were regulated by negative cooperativity in an aggregating system. Moreover, the driving force for asymmetry in human EGFR dimmers may arise from the intracellular region in EGFR (21). High-affinity EGFRs, which are correlated with Ras/MAPK and PI3K/Akt pathways (20), are more highly expressed in periportal than in PVH, resulting in DNA synthesis correlating to the EGFR expression level (15). We rep...

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Physioanatomic Considerations

Wanless

2017

Schiff's Diseases of the Liver

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The Effect of Denervation on Liver Regeneration in Partially Hepatectomized Rats

Cited by 13 publications

References 22 publications

Role of the Autonomic Nervous System in Rat Liver Regeneration

Role of the Autonomic Nervous System in Rat Liver Regeneration

Effect of aging on norepinephrine-related proliferative response in primary cultured periportal and perivenous hepatocytes

Physioanatomic Considerations

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