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Journal articles on the topic 'Hepatocyte growth facter'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2025

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1

FURUKAWA, M., Y. MAGAMI, D. NAKAYAMA, F. MORIYASU, T. NIKAIDO, and T. SAKAI. "Possible involvement of p21/waf1 in the growth of hepatocellular carcinoma cells by hepatocyte growth facter (HGF)." Gastroenterology 120, no. 5 (2001): A360. http://dx.doi.org/10.1016/s0016-5085(01)81791-1.

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2

Furukawa, Masaya, Yasushi Magami, Daiju Nakayama, Fuminori Moriyasu, Toshio Nikaido, and Toshiyuki Sakai. "Possible involvement of p21/waf1 in the growth of hepatocellular carcinoma cells by hepatocyte growth facter (HGF)." Gastroenterology 120, no. 5 (2001): A360. http://dx.doi.org/10.1016/s0016-5085(08)81791-x.

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3

Nagoshi, Sumiko, Shinichi Ota, and Kenji Fujiwara. "Polyamines may be involved in hepatocyte growth facter-stimulated restitution of rabbit gastric epithelial cells in primary culture." Gastroenterology 118, no. 4 (2000): A1281. http://dx.doi.org/10.1016/s0016-5085(00)80974-9.

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4

Gupta, Sanjeev, Pankaj Rajvanshi, Emma Aragona, Chang-Don Lee, Purnachandra R. Yerneni, and Robert D. Burk. "Transplanted hepatocytes proliferate differently after CCl4 treatment and hepatocyte growth factor infusion." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 3 (1999): G629—G638. http://dx.doi.org/10.1152/ajpgi.1999.276.3.g629.

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To understand regulation of transplanted hepatocyte proliferation in the normal liver, we used genetically marked rat or mouse cells. Hosts were subjected to liver injury by carbon tetrachloride (CCl4), to liver regeneration by a two-thirds partial hepatectomy, and to hepatocellular DNA synthesis by infusion of hepatocyte growth factor for comparative analysis. Transplanted hepatocytes were documented to integrate in periportal areas of the liver. In response to CCl4 treatments after cell transplantation, the transplanted hepatocyte mass increased incrementally, with the kinetics and magnitude

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Lilja, Helene, Pierre Blanc, Achilles A. Demetriou, and Jacek Rozga. "Response of Cultured Fetal and Adult Rat Hepatocytes to Growth Factors and Cyclosporine." Cell Transplantation 7, no. 3 (1998): 257–66. http://dx.doi.org/10.1177/096368979800700304.

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Hepatocyte transplantation is a promising alternative to orthotopic liver transplantation in experimental animal models with genetic disorders of liver metabolism and liver failure. Fetal hepatocytes have several characteristics that make them potentially suitable as donor cells. In contrast to adult hepatocytes, fetal hepatocytes are thought to be highly proliferative, which may facilitate engraftment, expansion of transplanted cell population, and gene transfer requiring active DNA synthesis. The present study was undertaken to evaluate the proliferative capacity of fetal and adult rat hepat

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6

Watanabe, Y., H. Osaki, and T. Akaike. "TNF-alpha bifunctionally induces proliferation in primary hepatocytes: role of cell anchorage and spreading." Journal of Immunology 159, no. 10 (1997): 4840–47. http://dx.doi.org/10.4049/jimmunol.159.10.4840.

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Abstract In the absence of a growth factor or an appropriate extracellular matrix (ECM), cells are arrested in the G0/G1 phase. In this report, we demonstrate the evidence that TNF-alpha induced DNA synthesis of primary mouse hepatocytes in vitro by activating two distinct pathways. TNF-alpha induced drastic spreading of hepatocytes on hydrophobic plastic, while the adhesion was not influenced. The effect was time and dose dependent. The cell spreading was accompanied by the phosphorylation of paxillin, indicating the stimulation of focal adhesion molecules. TNF-alpha-induced spreading of hepa

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7

Block, G. D., J. Locker, W. C. Bowen, et al. "Population expansion, clonal growth, and specific differentiation patterns in primary cultures of hepatocytes induced by HGF/SF, EGF and TGF alpha in a chemically defined (HGM) medium." Journal of Cell Biology 132, no. 6 (1996): 1133–49. http://dx.doi.org/10.1083/jcb.132.6.1133.

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Mature adult parenchymal hepatocytes, typically of restricted capacity to proliferate in culture, can now enter into clonal growth under the influence of hepatocyte growth factor (scatter factor) (HGF/SF), epidermal growth factor (EGF), and transforming growth factor alpha (TGFalpha) in the presence of a new chemically defined medium (HGM). The expanding populations of hepatocytes lose expression of hepatocyte specific genes (albumin, cytochrome P450 IIB1), acquire expression of markers expressed by bile duct epithelium (cytokeratin 19), produce TGFalpha and acidic FGF and assume a very simpli

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8

Wei, Miaomiao, Xinlong Yan, Xin Xin, Haiqiang Chen, Lingling Hou, and Jinhua Zhang. "Hepatocyte-Specific Smad4 Deficiency Alleviates Liver Fibrosis via the p38/p65 Pathway." International Journal of Molecular Sciences 23, no. 19 (2022): 11696. http://dx.doi.org/10.3390/ijms231911696.

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Liver fibrosis is a wound-healing response caused by the abnormal accumulation of extracellular matrix, which is produced by activated hepatic stellate cells (HSCs). Most studies have focused on the activated HSCs themselves in liver fibrosis, and whether hepatocytes can modulate the process of fibrosis is still unclear. Sma mothers against decapentaplegic homologue 4 (Smad4) is a key intracellular transcription mediator of transforming growth factor-β (TGF-β) during the development and progression of liver fibrosis. However, the role of hepatocyte Smad4 in the development of fibrosis is poorl

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9

Bilezikçi, Banu, Asuman Nihan Haberal, and Beyhan Demirhan. "Hepatocyte Growth Factor in Patients with Three Different Stages of Chronic Liver Disease including Hepatocellular Carcinoma, Cirrhosis and Chronic Hepatitis: An Immunohistochemical Study." Canadian Journal of Gastroenterology 15, no. 3 (2001): 159–65. http://dx.doi.org/10.1155/2001/930629.

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BACKGROUND AND AIMS: The specific role of hepatocyte growth factor in liver disease is unknown. The presence and density of this factor in patients with three different stages of liver disease were investigated, with the aim of assessing its prognostic significance.PATIENTS AND METHODS: Liver specimens from patients with chronic hepatitis (n=20), cirrhosis (n=20), hepatocellular carcinoma (n=30) and normal livers (n=20) were immunohistochemically stained to determine the presence and density of hepatocyte growth factor.RESULTS: There were significantly more hepatocyte growth factor-positive Ku

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10

Liu, Ke-Xin, Yukio Kato, Tai-Ichi Kaku, Kunio Matsumoto, Toshikazu Nakamura, and Yuichi Sugiyama. "Protamine enhances the proliferative activity of hepatocyte growth factor in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 1 (1998): G21—G28. http://dx.doi.org/10.1152/ajpgi.1998.274.1.g21.

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The effect of protamine on the proliferative activity of hepatocyte growth factor (HGF) was examined in α-naphthyl isothiocyanate-intoxicated rats. Protamine preinjection increased the hepatocyte labeling index induced by HGF four- to fivefold. A similar effect was also observed in partially hepatectomized rats. Because a cell surface heparin-like substance can bind to HGF and protamine has an affinity for heparin, protamine may affect HGF pharmacokinetics. In fact, protamine injection caused a transient increase in plasma HGF concentrations after administration of HGF and, in vitro, protamine

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11

Scott, C. D., and R. C. Baxter. "Synthesis of the acid-labile subunit of the growth-hormone-dependent insulin-like-growth-factor-binding protein complex by rat hepatocytes in culture." Biochemical Journal 275, no. 2 (1991): 441–46. http://dx.doi.org/10.1042/bj2750441.

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Insulin-like growth factors (IGFs) circulate predominantly in a growth-hormone-dependent ternary complex of 125-150 kDa. This study investigates the production of the alpha-subunit of this complex, an acid-labile glycoprotein without intrinsic IGF-binding activity, which binds to the IGF-binding protein IGFBP-3 in the presence of IGFs. Medium conditioned by primary cultures of rat hepatocytes produced alpha-subunit with similar complex-forming activity to purified rat serum alpha-subunit. Bovine growth hormone stimulated hepatocyte production of both IGF-I and alpha-subunit. IGF-I tracer bound

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12

Gómez-Aristizábal, Alejandro, and John Edward Davies. "The effects of human umbilical cord perivascular cells on rat hepatocyte structure and functional polarity." Biochemistry and Cell Biology 91, no. 3 (2013): 140–47. http://dx.doi.org/10.1139/bcb-2012-0079.

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Hepatocyte culture is a useful tool for the study of their biology and the development of bioartificial livers. However, many challenges have to be overcome since hepatocytes rapidly lose their normal phenotype in vitro. We have recently demonstrated that human umbilical cord perivascular cells (HUCPVCs) are able to provide support to hepatocytes. In the present study we go further into exploring the effects that HUCPVCs have in the functional polarization, and both the internal and external organization, of hepatocytes. Also, we investigate HUCPVC–hepatocyte crosstalk by tracking both the eff

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13

Ju, Wenjun, Atsushi Ogawa, Joerg Heyer, et al. "Deletion of Smad2 in Mouse Liver Reveals Novel Functions in Hepatocyte Growth and Differentiation." Molecular and Cellular Biology 26, no. 2 (2006): 654–67. http://dx.doi.org/10.1128/mcb.26.2.654-667.2006.

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ABSTRACT Smad family proteins Smad2 and Smad3 are activated by transforming growth factor β (TGF-β)/activin/nodal receptors and mediate transcriptional regulation. Although differential functional roles of Smad2 and Smad3 are apparent in mammalian development, the relative functional roles of Smad2 and Smad3 in postnatal systems remain unclear. We used Cre/loxP-mediated gene targeting for hepatocyte-specific deletion of Smad2 (S2HeKO) in adult mice and generated hepatocyte-selective Smad2/Smad3 double knockouts by intercrossing AlbCre/Smad2f/f (S2HeKO) and Smad3-deficient Smad3ex8/ex8 (S3KO) m

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14

Boylan, J. M., and P. A. Gruppuso. "In vitro and in vivo regulation of hepatic mitogen-activated protein kinases in fetal rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 6 (1994): G1078—G1086. http://dx.doi.org/10.1152/ajpgi.1994.267.6.g1078.

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We have studied the role of mitogen-activated protein (MAP) kinases in fetal hepatocyte growth in vitro and in vivo. With myelin basic protein (MBP) as the phosphate acceptor, kinase activity in cultured fetal hepatocyte lysates increased fourfold after exposure to transforming growth factor-alpha (TGF-alpha) for 10 min. This TGF-alpha-responsive MBP kinase activity was accounted for by five distinct MAP kinase isoforms detected by Western immunoblotting. All had negligible activity in cultured fetal hepatocytes under basal conditions. Treatment of fetal hepatocytes with hepatocyte growth fact

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15

Kim, T. H., H. M. Lee, H. Utsonomiya, et al. "Enhanced survival of transgenic hepatocytes expressing hepatocyte growth factor in hepatocyte tissue engineering." Transplantation Proceedings 29, no. 1-2 (1997): 858–60. http://dx.doi.org/10.1016/s0041-1345(96)00169-8.

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16

Priego, Teresa, Miriam Granado, Estibaliz Castillero, Ana Isabel Martín, M. Ángeles Villanúa, and Asunción López-Calderón. "Nitric oxide production by hepatocytes contributes to the inhibitory effect of endotoxin on insulin-like growth factor I gene expression." Journal of Endocrinology 190, no. 3 (2006): 847–56. http://dx.doi.org/10.1677/joe.1.06938.

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We tested whether endotoxin (lipopolysaccharide, LPS) inhibits IGF-I gene expression in hepatocytes and the possible role of Kupffer cells and nitric oxide (NO) in this effect. LPS decreased IGF-I mRNA in hepatocyte cultures and increased the nitrite + nitrate levels in the culture medium. Furthermore, there was a negative correlation between the IGF-I mRNA and the nitrite+nitrate levels. When hepatocytes were cocultured with Kupffer cells, the inhibitory effect of LPS on IGF-I mRNA was higher than in hepatocyte cultures, but the stimulatory effect on nitrite+nitrate was similar in both condit

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17

Sponsel, H. T., P. S. Guzelian, S. E. Brown, et al. "Mechanisms of recovery from mechanical injury of cultured rat hepatocytes." American Journal of Physiology-Cell Physiology 271, no. 3 (1996): C721—C727. http://dx.doi.org/10.1152/ajpcell.1996.271.3.c721.

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The mechanism(s) whereby hepatocytes restore denuded areas remains unknown. We therefore studied the recovery of denuded areas made in monolayers of primary cultures of rat hepatocytes. Minimal recovery occurred in cells plated on plastic. Plating on Matrigel produced modest recovery (25% at 24 h), whereas plating on a type I collagen substrate resulted in > 70% recovery at 24 h. The rate of recovery on collagen could be attenuated by a monoclonal antibody directed against the extracellular domain of the beta 1-integrin subunit. Monoclonal antibodies directed against CD44 (the hyaluron rece

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18

Michalopoulos, George K. "Principles of Liver Regeneration and Growth Homeostasis." Comprehensive Physiology 3, no. 1 (2013): 485–513. https://doi.org/10.1002/j.2040-4603.2013.tb00493.x.

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AbstractLiver regeneration is perhaps the most studied example of compensatory growth aimed to replace loss of tissue in an organ. Hepatocytes, the main functional cells of the liver, manage to proliferate to restore mass and to simultaneously deliver all functions hepatic functions necessary to maintain body homeostasis. They are the first cells to respond to regenerative stimuli triggered by mitogenic growth factor receptors MET (the hepatocyte growth factor receptor] and epidermal growth factor receptor and complemented by auxiliary mitogenic signals induced by other cytokines. Termination

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19

Schrum, Laura W., Mark A. Bird, Olga Salcher та ін. "Autocrine expression of activated transforming growth factor-β1 induces apoptosis in normal rat liver". American Journal of Physiology-Gastrointestinal and Liver Physiology 280, № 1 (2001): G139—G148. http://dx.doi.org/10.1152/ajpgi.2001.280.1.g139.

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The aim of this study was to determine the differential effects of latent and activated transforming growth factor (TGF)-β1in growth control of normal and proliferating hepatocytes in vivo. Rats were injected with adenoviruses expressing control transgenes (Ctrl), latent TGF-β1 [TGF-β(L)], or activated TGF-β1 [TGF-β(A)]. Additional animals underwent two-thirds partial hepatectomy (PH) 24 h after injection. Increased hepatocyte apoptosis was observed in TGF-β(A)-injected but not TGF-β(L)-injected animals 24 h postinjection (10.5%) compared with Ctrl animals (0.37%). The percent of apoptotic cel

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20

Huitfeldt, H. S., E. Skarpen, B. Lindeman, R. Becher, E. V. Thrane, and P. E. Schwarze. "Differential distribution of Met and epidermal growth factor receptor in normal and carcinogen-treated rat liver." Journal of Histochemistry & Cytochemistry 44, no. 3 (1996): 227–33. http://dx.doi.org/10.1177/44.3.8648082.

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Transforming growth factor-alpha (TGF-alpha) and hepatocyte growth factor (HGF) are strong hepatocyte mitogens and important regulators of liver regeneration. The TGF-alpha receptor EGFr appears primarily to mediate a proliferative signal, whereas mitogenic, motogenic, and morphogenic effects have been attributed to activation of the HGF receptor Met. We have studied the localization of Met and EGFr in normal and carcinogen-treated rat livers. Oval cells and preneoplastic lesions were induced by diethylnitrosamine initiation, followed by promotion with 2-acetylaminofluorene combined with a par

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Varghese, Divya S., Thilina Thejinda Alawathugoda, and Suraiya A. Ansari. "Fine Tuning of Hepatocyte Differentiation from Human Embryonic Stem Cells: Growth Factor vs. Small Molecule-Based Approaches." Stem Cells International 2019 (January 22, 2019): 1–18. http://dx.doi.org/10.1155/2019/5968236.

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Human embryonic stem cells (hESCs) are being utilized in diverse areas of studies such as development and disease modeling, cell replacement therapy, or drug toxicity testing because of their potential to be differentiated into any cell type in the body. The directed differentiation of hESCs into hepatocytes could provide an invaluable source of liver cells for various liver-based applications. Therefore, several protocols have been established in the past for hESC-hepatocyte differentiation based on the knowledge of signaling pathways and growth factors involved in different stages of embryon

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New-Aaron, Moses, Siva Sankar Koganti, Murali Ganesan, et al. "Hepatocyte-Specific Triggering of Hepatic Stellate Cell Profibrotic Activation by Apoptotic Bodies: The Role of Hepatoma-Derived Growth Factor, HIV, and Ethanol." International Journal of Molecular Sciences 24, no. 6 (2023): 5346. http://dx.doi.org/10.3390/ijms24065346.

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Liver disease is one of the leading comorbidities in HIV infection. The risk of liver fibrosis development is potentiated by alcohol abuse. In our previous studies, we reported that hepatocytes exposed to HIV and acetaldehyde undergo significant apoptosis, and the engulfment of apoptotic bodies (ABs) by hepatic stellate cells (HSC) potentiates their pro-fibrotic activation. However, in addition to hepatocytes, under the same conditions, ABs can be generated from liver-infiltrating immune cells. The goal of this study is to explore whether lymphocyte-derived ABs trigger HSC profibrotic activati

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Park, Jung-Hyun, Kyung-Hyun Kim, Soo-Jung Kim та ін. "Effect of Bee Venom on Transforming Growth Factor–β1-Treated Hepatocytes". International Journal of Toxicology 29, № 1 (2010): 49–56. http://dx.doi.org/10.1177/1091581809353948.

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Bee venom (BV) has been used as treatment against a wide variety of ailments, including inflammatory diseases. Various studies have demonstrated anti-inflammatory and anticancer effects of BV. Transforming growth factor (TGF)–β1 induces hepatocyte apoptosis via the mitochondrial permeability transition. However, there is no evidence or information regarding the antiapoptotic effect of BV on hepatocytes. The authors investigated the antiapoptotic effect of BV on TGF-β1-treated hepatocytes. The results showed significant protection from DNA damage by BV treatment compared to corresponding TGF-β1

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Sharma, Shiv K. "Hepatocyte Growth Factor in Synaptic Plasticity and Alzheimer's Disease." Scientific World JOURNAL 10 (2010): 457–61. http://dx.doi.org/10.1100/tsw.2010.49.

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The hepatocyte growth factor (HGF) was initially identified as a protein that promoted growth of hepatocytes. It regulates proliferation and survival of different types of cells. HGF signaling, which is initiated by its binding to a receptor tyrosine kinase, plays critical roles during development. HGF and its receptor are also present in brain cells. This review describes the role of HGF in hippocampal neurons, synaptic plasticity, and the memory impairment condition, Alzheimer's disease.

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Iida, Ichiei, Kohei Johkura, Ruifeng Teng, et al. "Immunohistochemical Localization of Hepatocyte Growth Factor Activator (HGFA) in Developing Mouse Liver Tissues: Heterogeneous Distribution of HGFA Protein." Journal of Histochemistry & Cytochemistry 51, no. 9 (2003): 1139–49. http://dx.doi.org/10.1177/002215540305100904.

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Hepatocyte growth factor activator (HGFA) can activate the single-chain hepatocyte growth factor (HGF) required for embryonic development. We studied the immunohistochemical (IHC) localization of HGFA in adult mouse liver and its developmental changes from embryonic day 12 to postnatal day 30. A heterogeneous distribution of HGFA was observed in adult liver tissues. The hepatocytes around the hepatic veins were preferentially positive for HGFA, whereas those in other areas were negative. Depending on the vascular diameter, the hepatic veins were bordered by a one- to three-cell-thick layer of

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26

Metcalfe, A. M. J., P. Phillips, R. M. Dixon, and G. K. Radda. "Vasopressin synergistically stimulates DNA synthesis in normal and regenerating rat liver cell cultures in the presence of hepatocyte growth factor." Journal of Molecular Endocrinology 18, no. 2 (1997): 161–66. http://dx.doi.org/10.1677/jme.0.0180161.

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ABSTRACT Liver regeneration is significantly impaired in rats with both α-adrenergic hepatic denervation and hereditary vasopressin deficiency. This may implicate a direct role for these agonists in the process of compensatory hyperplasia. The mitogenic capacities of norepinephrine, vasopressin and hepatocyte growth factor (HGF), either alone or in combination were investigated by [3H]thymidine incorporation into hepatocyte cultures prepared from normal and regenerating rat livers. The results show that normal hepatocytes incorporate less [3H]thymidine in response to HGF than do regenerating h

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Skouteris, G. G., та M. McMenamin. "Transforming growth factor-α-induced DNA synthesis and c-myc expression in primary rat hepatocyte cultures is modulated by indomethacin". Biochemical Journal 281, № 3 (1992): 729–33. http://dx.doi.org/10.1042/bj2810729.

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Primary hepatocytes stimulated with epidermal growth factor (EGF) secrete prostaglandins into the culture medium as soon as 1 h after the addition of the EGF. Transforming growth factor-alpha (TGF alpha), a potent hepatocyte mitogen, shares the same receptor with EGF, and its expression is increased after partial hepatectomy. TGF alpha is also secreted in culture. We have observed that TGF alpha induced hepatocyte DNA synthesis (30 h after addition) and at the same time stimulated the production of prostaglandins E2 and F2 alpha by the cultured hepatocytes. Indomethacin at 20-100 microM inhibi

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28

Sharma, Santosh Kumar, Amar Nath Chatterjee, and Bashir Ahmad. "Effect of Antiviral Therapy for HCV Treatment in the Presence of Hepatocyte Growth Factor." Mathematics 11, no. 3 (2023): 751. http://dx.doi.org/10.3390/math11030751.

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The effect of antiviral therapy during Hepatitis C Virus (HCV) infection is the focus of this study. HCV infection destroys healthy hepatocyte cells in the human liver, causing cirrhosis and hepatocellular carcinoma. We introduce a cell-population model representing the long-term dynamics of HCV infection in response to antiviral drug therapies. The proliferation of existing cells can create hepatocyte cells in the system. Such models are based on the dynamics of susceptible hepatocytes, infected hepatocytes and HCV with interactive dynamics, which can give a complete understanding of the host

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Minnis-Lyons, Sarah E., Sofía Ferreira-González, Niya Aleksieva, et al. "Notch-IGF1 signaling during liver regeneration drives biliary epithelial cell expansion and inhibits hepatocyte differentiation." Science Signaling 14, no. 688 (2021): eaay9185. http://dx.doi.org/10.1126/scisignal.aay9185.

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In the adult liver, a population of facultative progenitor cells called biliary epithelial cells (BECs) proliferate and differentiate into cholangiocytes and hepatocytes after injury, thereby restoring liver function. In mammalian models of chronic liver injury, Notch signaling is essential for bile duct formation from these cells. However, the continual proliferation of BECs and differentiation of hepatocytes in these models have limited their use for determining whether Notch signaling is required for BECs to replenish hepatocytes after injury in the mammalian liver. Here, we used a temporal

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Rippe, R. A., D. A. Brenner, and H. L. Leffert. "DNA-mediated gene transfer into adult rat hepatocytes in primary culture." Molecular and Cellular Biology 10, no. 2 (1990): 689–95. http://dx.doi.org/10.1128/mcb.10.2.689-695.1990.

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Proliferation-competent and differentiation-competent adult rat hepatocytes in primary culture were investigated for their ability to express reporter genes (firefly luciferase, bacterial chloramphenicol acetyltransferase, and bacterial beta-galactosidase) driven by tumor virus or eucaryotic promoters that vary in transcriptional efficiency and tissue specificity. Supercoiled plasmid DNA molecules were introduced into the cells by the calcium phosphate coprecipitation protocol of C. Chen and H. Okayama (Mol. Cell. Biol. 7:2745-2752, 1987). Reporter gene expression was virtually restricted to h

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Rippe, R. A., D. A. Brenner, and H. L. Leffert. "DNA-mediated gene transfer into adult rat hepatocytes in primary culture." Molecular and Cellular Biology 10, no. 2 (1990): 689–95. http://dx.doi.org/10.1128/mcb.10.2.689.

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Proliferation-competent and differentiation-competent adult rat hepatocytes in primary culture were investigated for their ability to express reporter genes (firefly luciferase, bacterial chloramphenicol acetyltransferase, and bacterial beta-galactosidase) driven by tumor virus or eucaryotic promoters that vary in transcriptional efficiency and tissue specificity. Supercoiled plasmid DNA molecules were introduced into the cells by the calcium phosphate coprecipitation protocol of C. Chen and H. Okayama (Mol. Cell. Biol. 7:2745-2752, 1987). Reporter gene expression was virtually restricted to h

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32

Pierce, A. L., H. Fukada, and W. W. Dickhoff. "Metabolic hormones modulate the effect of growth hormone (GH) on insulin-like growth factor-I (IGF-I) mRNA level in primary culture of salmon hepatocytes." Journal of Endocrinology 184, no. 2 (2005): 341–49. http://dx.doi.org/10.1677/joe.1.05892.

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Liver production of insulin-like growth factor-I (IGF-I) is a major point of control in the growth hormone (GH)/IGF axis, the endocrine system regulating body growth in fishes and other vertebrates. Pituitary GH stimulates hepatocyte production of IGF-I; however, in catabolic states, hepatocyte GH resistance results in decreases in liver IGF-I production. To investigate endocrine mechanisms leading to the development of hepatocyte GH resistance, we examined the regulation of IGF-I mRNA level by GH and metabolic hormones in primary culture of salmon hepatocytes. Cells were cultured in RPMI medi

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Kaneko, Akira, Norio Hayashi, Yuji Tanaka, et al. "Activation of Na+/H+ exchanger by hepatocyte growth factor in hepatocytes." Hepatology 22, no. 2 (1995): 629–36. http://dx.doi.org/10.1002/hep.1840220237.

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Rowell, D. L., L. Eckmann, M. B. Dwinell, et al. "Human hepatocytes express an array of proinflammatory cytokines after agonist stimulation or bacterial invasion." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 2 (1997): G322—G332. http://dx.doi.org/10.1152/ajpgi.1997.273.2.g322.

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Inflammatory cells infiltrate the liver in response to microbial infection or hepatic injury. To assess the potential role hepatocytes may play in initiating or amplifying the acute inflammatory response in the liver, we used three human hepatocyte cell lines and primary human hepatocyte cultures to characterize the repertoire of cytokines that can be expressed and regulated in hepatocytes in response to agonist stimulation or bacterial infection. As reported herein, a proinflammatory cytokine gene program that includes C-X-C and C-C chemokines [interleukin-8(IL-8), growth related (GRO)-alpha,

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35

Li, Zhaodong, Shinya Mizuno, and Toshikazu Nakamura. "Antinecrotic and antiapoptotic effects of hepatocyte growth factor on cholestatic hepatitis in a mouse model of bile-obstructive diseases." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 2 (2007): G639—G646. http://dx.doi.org/10.1152/ajpgi.00292.2006.

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Cholestasis, an impairment of bile outflux, frequently occurs in liver diseases. In this process, an overaccumulation of bile acids causes hepatocyte necrosis and apoptosis, leading to advanced hepatitis. Hepatocyte growth factor (HGF) is mitogenic toward hepatocytes, but it is still unclear whether HGF has physiological and therapeutic functions during the progression of cholestasis. Using anti-HGF IgG or recombinant HGF in mice that had undergone bile duct ligation (BDL), we investigated the involvement of HGF in cholestasis-induced hepatitis. After the BDL surgery, HGF and c-Met mRNA levels

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Runge, Dorothee M., Dieter Runge, Kenneth Dorko, et al. "Epidermal growth factor- and hepatocyte growth factor-receptor activity in serum-free cultures of human hepatocytes." Journal of Hepatology 30, no. 2 (1999): 265–74. http://dx.doi.org/10.1016/s0168-8278(99)80073-7.

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Uetake, Akiko, Atsuya Takeda, Naoyuki Shigematsu, et al. "Multiple myeloma relapse in the irradiated liver: involvement of hepatocyte growth factor akin to that after hepatocyte transplantation." Journal of Radiotherapy in Practice 11, no. 4 (2012): 271–73. http://dx.doi.org/10.1017/s1460396912000131.

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AbstractWe described a rare case of multiple myeloma in a 60-year-old man, in whom relapse limited to the irradiated area in the left lobe of the liver developed following radiotherapy for lesions in 11th and 12th thoracic spines. Immunohistochemical analysis revealed expression of hepatocyte growth factor (HGF) and hepatocyte growth factor receptor (c-Met) in the hepatocytes in the irradiated area of the liver. We speculate that the malignant plasma cells might have proliferated in response to local increase of HGF production in the irradiated liver. The role of HGF in the extraosseous spread

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Strain, A. J., and J. M. Neuberger. "Hepatocyte growth factor." Gut 33, no. 2 (1992): 286–87. http://dx.doi.org/10.1136/gut.33.2.286.

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39

Mason, Robert J. "Hepatocyte Growth Factor." American Journal of Respiratory Cell and Molecular Biology 26, no. 5 (2002): 517–20. http://dx.doi.org/10.1165/ajrcmb.26.5.f239.

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Michalopoulos, George K., and Reza Zarnegar. "Hepatocyte growth factor." Hepatology 15, no. 1 (1992): 149–55. http://dx.doi.org/10.1002/hep.1840150125.

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Holt, Margrethe Flesvig, Annika E. Michelsen, August Flø, et al. "Hepatocyte Growth Factor." JACC: Advances 4, no. 6 (2025): 101828. https://doi.org/10.1016/j.jacadv.2025.101828.

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Choi, Jong Hoon, Lorena Loarca, Jose M. De Hoyos-Vega, et al. "Microfluidic confinement enhances phenotype and function of hepatocyte spheroids." American Journal of Physiology-Cell Physiology 319, no. 3 (2020): C552—C560. http://dx.doi.org/10.1152/ajpcell.00094.2020.

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A number of cell culture approaches have been described for maintenance of primary hepatocytes. Forming hepatocytes into three-dimensional (3-D) spheroids is one well-accepted method for extending epithelial phenotype of these cells. Our laboratory has previously observed enhanced function of two-dimensional (2-D, monolayer) hepatocyte cultures in microfluidic devices due to increased production of several hepato-inductive growth factors, including hepatocyte growth factor (HGF). In the present study, we wanted to test a hypothesis that culturing hepatocyte spheroids (3-D) in microfluidic devi

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Domínguez-Pérez, Mayra, Natalia Nuño-Lámbarri, Denise Clavijo-Cornejo, et al. "Hepatocyte Growth Factor Reduces Free Cholesterol-Mediated Lipotoxicity in Primary Hepatocytes by Countering Oxidative Stress." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/7960386.

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Cholesterol overload in the liver has shown toxic effects by inducing the aggravation of nonalcoholic fatty liver disease to steatohepatitis and sensitizing to damage. Although the mechanism of damage is complex, it has been demonstrated that oxidative stress plays a prominent role in the process. In addition, we have proved that hepatocyte growth factor induces an antioxidant response in hepatic cells; in the present work we aimed to figure out the protective effect of this growth factor in hepatocytes overloaded with free cholesterol. Hepatocytes from mice fed with a high-cholesterol diet we

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Lee, Joonyong, Veronica Garcia, Shashank Manohar Nambiar, Huaizhou Jiang, and Guoli Dai. "Pregnancy facilitates maternal liver regeneration after partial hepatectomy." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 4 (2020): G772—G780. http://dx.doi.org/10.1152/ajpgi.00125.2019.

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Liver resection induces robust liver regrowth or regeneration to compensate for the lost tissue mass. In a clinical setting, pregnant women may need liver resection without terminating pregnancy in some cases. However, how pregnancy affects maternal liver regeneration remains elusive. We performed 70% partial hepatectomy (PH) in nonpregnant mice and gestation day 14 mice, and histologically and molecularly compared their liver regrowth during the next 4 days. We found that compared with the nonpregnant state, pregnancy altered the molecular programs driving hepatocyte replication, indicated by

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Gupta, Devendra Kumar, Neetu Singh та Dinesh Kumar Sahu. "Article Commentary: TGF-β Mediated Crosstalk between Malignant Hepatocyte and Tumor Microenvironment in Hepatocellular Carcinoma". Cancer Growth and Metastasis 7 (січень 2014): CGM.S14205. http://dx.doi.org/10.4137/cgm.s14205.

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In this article, we have reviewed current literature regarding the regulation of hepatocellular carcinoma (HCC) by the interaction of malignant hepatocytes and their tissue environment through cytokine signaling, here represented by transforming growth factor-beta (TGF-β) signaling. We have discussed responses of TGF-β signaling in transition of hepatic stellate cells to myofibroblasts (MFBs), recruitment of tumor-associated macrophages (TAMs), and enrichment of tumor-associated endothelial cells (TECs). The malignant hepatocytes also secrete various factors such as platelet-derived growth fac

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Woo, Jin-Hee. "The Effects of Exercise on Neurotrophins, Hepatocyte Growth Factor (HGF), and Oxidative Stress in Obese Children." Journal of Life Science 22, no. 5 (2012): 569–74. http://dx.doi.org/10.5352/jls.2012.22.5.569.

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Roos, F., A. M. Ryan, S. M. Chamow, G. L. Bennett, and R. H. Schwall. "Induction of liver growth in normal mice by infusion of hepatocyte growth factor/scatter factor." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 2 (1995): G380—G386. http://dx.doi.org/10.1152/ajpgi.1995.268.2.g380.

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Hepatocyte growth factor/scatter factor (HGF/SF) is a potent stimulator of DNA synthesis in a variety of epithelial cells, including hepatocytes, and has been implicated in liver regeneration. We show here that combining dextran sulfate with HGF/SF markedly increases the plasma concentrations of HGF/SF that are achieved during intraperitoneal infusion. Three days of administration of HGF/SF by this mechanism caused a dose-dependent increase in liver wet weight. Mitotic figures were rarely observed in control livers but were abundant in livers exposed to HGF/SF, and liver DNA content was elevat

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Kaibori, Masaki, A.-Hon Kwon, Shigeru Teshima, et al. "Hepatocyte growth factor inhibits insulin-stimulated glycogen synthesis in primary cultured hepatocytes." Journal of Hepatology 38, no. 4 (2003): 407–13. http://dx.doi.org/10.1016/s0168-8278(02)00455-5.

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Valdés-Arzate, Argelia, Armando Luna, Leticia Bucio, et al. "Hepatocyte growth factor protects hepatocytes against oxidative injury induced by ethanol metabolism." Free Radical Biology and Medicine 47, no. 4 (2009): 424–30. http://dx.doi.org/10.1016/j.freeradbiomed.2009.05.014.

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Wang, Bin, Cuihua Gao та Katherine Parker Ponder. "C/EBPβ contributes to hepatocyte growth factor-induced replication of rodent hepatocytes". Journal of Hepatology 43, № 2 (2005): 294–302. http://dx.doi.org/10.1016/j.jhep.2005.02.029.

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