Journal articles: 'Hepatocyte growth facter'

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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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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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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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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 of DNA synthesis being similar to those of host hepatocytes. In contrast, when cells were transplanted 24 h after CCl4 administration, transplanted hepatocytes appeared to be injured and most cells were rapidly cleared. When hepatocyte growth factor was infused into the portal circulation either subsequent to or before cell transplantation and engraftment, transplanted cell mass did not increase, although DNA synthesis rates increased in cultured primary hepatocytes as well as in intact mouse and rat livers. These data suggested that procedures causing selective ablation of host hepatocytes will be most effective in inducing transplanted cell proliferation in the normal liver. The number of transplanted hepatocytes was not increased in the liver by hepatocyte growth factor administration. Repopulation of the liver with genetically marked hepatocytes can provide effective reporters for studying liver growth control in the intact animal.

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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 hepatocytes under standardized culture conditions. Fetal (20 days of gestation) and adult hepatocytes were cultured in serum-free media at low densities and treated with growth factors. Proliferation was assessed by [3H]-thymidine incorporation and cell cycle analysis by flow cytometry. In nonstimulated cells, DNA synthesis at 4 h was about × 100 higher and after 10 days in culture ×20 higher in fetal compared to adult hepatocytes. When epidermal growth factor (EGF) was added, maximal DNA synthesis in fetal hepatocytes was seen at 48 h, whereas in adult hepatocytes at 72 h. For adult hepatocytes, the average increase compared to untreated cells was × 13.8 with EGF, ×18.5 with transforming growth factor alpha (TGF-α), and ×7.6 with hepatocyte growth factor (HGF). For fetal hepatocytes, the increase was twofold with either EGF, TGF-α or HGF. EGF-, TGF-α- and HGF-dependent DNA synthesis was inhibited by transfroming growth factor beta-1 (TGF-β1) in both fetal and adult hepatocyte cultures; this antiproliferative effect was significantly stronger in adult hepatocyte cultures. With cyclosporine, EGF-, TGF-α- and HGF-dependent DNA synthesis in fetal hepatocyte cultures decreased by 36–46%, whereas in adult hepatocytes by 19–27%. These results show that in contrast to adult hepatocytes, fetal hepatocytes have high spontaneous proliferative activity independently of growth factors and are relatively resistant to the inhibitory effect of TGF-β1. It was also found that cyclosporine suppresses proliferation of cultured fetal hepatocytes.

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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 simplified morphologic phenotype by electron microscopy. A major change associated with this transition is the decrease in ratio between transcription factors C/EBPalpha and C/EBPbeta, as well as the emergence in the proliferating hepatocytes of transcription factors AP1, NFkappaB. The liver associated transcription factors HNFI, HNF3, and HNF4 are preserved throughout this process. After population expansion and clonal growth, the proliferating hepatocytes can return to mature hepatocyte phenotype in the presence of EHS gel (Matrigel). This includes complete restoration of electron microscopic structure and albumin expression. The hepatocyte cultures however can instead be induced to form acinar/ductular structures akin to bile ductules (in the presence of HGF/SF and type I collagen). These transformations affect the entire population of the hepatocytes and occur even when DNA synthesis is inhibited. Similar acinar/ductular structures are seen in embryonic liver when HGF/SF and its receptor are expressed at high levels. These findings strongly support the hypothesis that mature hepatocytes can function as or be a source of bipotential facultative hepatic stem cells (hepatoblasts). These studies also provide evidence for the growth factor and matrix signals that govern these complex phenotypic transitions of facultative stem cells which are crucial for recovery from acute and chronic liver injury.

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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 Kupffer and Ito cells in all three diseased groups than in the control group. Also, there was significantly more positive staining in chronic hepatitis specimens than in specimens from the cirrhosis, hepatocellular carcinoma and control groups (P<0.05). The hepatoma cells in 10 of the hepatocellular carcinoma cases stained positive, but none of the hepatocytes in the chronic hepatitis, cirrhosis and normal liver specimens stained. It was only possible to assess nonmalignant hepatocytes adjacent to the hepatocellular carcinoma in the four resection specimens, and no staining for hepatocyte growth factor was observed in these areas. There was no statistical association between density of hepatocyte growth factor and histological activity index in chronic hepatitis, or between density of hepatocyte growth factor and grade of hepatocellular carcinoma.CONCLUSIONS: Similar to some previous reports, this study revealed that hepatoma cells can also express this growth factor. Immunohistochemical detection of hepatocyte growth factor may prove to be a useful method of diagnosing hepatocellular carcinoma in challenging cases.

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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 eluted HGF prebound to heparin-Sepharose. Protamine also reduced the plasma clearance of HGF and increased 2.5-fold the exposure of hepatocytes to HGF in vivo. The enhancing effect of protamine on the mitogenic response of hepatocytes to HGF was also observed in vitro (∼2-fold after protamine pretreatment compared with HGF alone), suggesting that the enhancing effect of protamine on HGF-induced liver regeneration results from dual effects exerted by protamine 1) lowering the overall elimination of HGF and 2) directly stimulating hepatocyte mitosis induced by HGF.

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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 to pure rat IGFBP-3 was converted from approx. 60 kDa to 150 kDa by serum alpha-subunit, whole rat serum or rat hepatocyte culture medium; this converting activity was destroyed by transient acidification. In contrast, IGF-I bound to hepatocyte-medium IGF-binding proteins could not be converted into a high-molecular-mass from by purified rat serum alpha-subunit. Rat serum and hepatocyte-medium alpha-subunit appeared identical by electrophoretic analysis, since reaction of either with cross-linked IGF-I.IGFBP-3 tracer resulted in bands of molecular mass 130 kDa and 160 kDa, probably representing intact and partially deglycosylated complexes. However, IGF-binding proteins in rat serum and hepatocyte medium were different, in that affinity labelling of medium binding proteins, depleted of endogenous IGFs, showed no evidence of the 50-60 kDa cluster of bands characteristic of rat serum IGFBP-3. We conclude that rat hepatocytes in primary culture produce alpha-subunit similar to that in rat serum; however, alpha-subunit is unable to form ternary complexes with hepatocyte IGF-binding proteins, since cultured hepatocytes do not secrete IGFBP-3.

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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 effects of HUCPVCs on hepatocyte transcription factors and those of hepatocytes on the expression of hepatotrophic factors in HUCPVCs. Our results show that HUCPVCs maintain the functional polarity of hepatocytes ex vivo, as judged by the secretion of fluorescein into bile canaliculi, for at least 40 days. Transmission electron microscopy revealed that hepatocytes in coculture organize in an organoid-like structure embedded in extracellular matrix surrounded by HUCPVCs. In coculture, hepatocytes displayed a higher expression of C/EBPα, implicated in maintenance of the mature hepatocyte phenotype, and HUCPVCs upregulated hepatocyte growth factor and Jagged1 indicating that these genes may play important roles in HUCPVC–hepatocyte interactions.

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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) mice. All strains were viable and had normal adult liver. However, necrogenic CCL4-induced hepatocyte proliferation was significantly increased in S2HeKO compared to Ctrl and S3KO livers, and transplanted S2HeKO hepatocytes repopulated recipient liver at dramatically increased rates compared to Ctrl hepatocytes in vivo. Using primary hepatocytes, we found that TGF-β-induced G1 arrest, apoptosis, and epithelial-to-mesenchymal transition in Ctrl and S2HeKO but not in S3KO hepatocytes. Interestingly, S2HeKO cells spontaneously acquired mesenchymal features characteristic of epithelial-to-mesenchymal transition (EMT). Collectively, these results demonstrate that Smad2 suppresses hepatocyte growth and dedifferentiation independent of TGF-β signaling. Smad2 is not required for TGF-β-stimulated apoptosis, EMT, and growth inhibition in hepatocytes.

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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 factor led to activation of the predominant isoforms, relative molecular weight (M(r)) = 42,000 and 44,000 in a manner indistinguishable from TGF-alpha, whereas insulin had no effect. All five of the immunoreactive MAP kinases were present in both fetal and adult liver homogenates. The M(r) = 42,000 and 44,000 isoforms were only minimally activated in vivo. We conclude that the mitogen-independent growth exhibited by fetal hepatocytes in primary culture is not associated with tonic activation of the MAP kinase system. Our data support the possibility that fetal hepatic growth may be, in part, independent of the action of growth factors as mediated via the MAP kinase system.

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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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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 receptor) and E-cadherin did not influence the rate of recovery. Recovery could be stimulated, in a dose-dependent fashion, by epidermal and hepatocyte growth factors. The effects of epidermal and hepatocyte growth factors to promote recovery occurred in the absence of 5-bromo-2'-deoxyuridine uptake, suggesting a proliferation-independent mechanism. Transforming growth factor-beta 1 inhibited recovery. Exposure to selected cytokines (interleukins 1 and 2), an adenine nucleotide [adenosine 5'-O-(3-thiotriphosphate)], adenosine, pertussis toxin, and selected agents that bind to fibronectin and other matrix component adhesive sites (heparin and the RGD peptide) did not influence the rate of recovery of hepatocytes. However, the peptide DGEA, which can bind to collagen adhesive sites, attenuated recovery. These studies demonstrate that primary cultures of rat hepatocytes require a particular type of extracellular matrix to renew denuded areas and that the beta 1-integrin subunit may be involved in this recovery process. Hepatocyte recovery of denuded areas can be modulated by growth factors in both a stimulatory (epidermal and hepatocyte growth factors) and an inhibitory (transforming growth factor-beta 1) fashion.

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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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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 conditions. The exogenous NO donated by S-nitroso-n-acetyl-d,l-penicillamide also decreased the IGF-I gene expression in hepatocyte cultures. In addition, two specific inducible NO synthase (iNOS) inhibitors, l-N6-(1-iminoethyl)lysine (l-NIL) and aminoguanidine, prevented the effect of LPS on nitrite+nitrate levels and on IGF-I gene expression in hepatocyte cultures. These data indicate that iNOS-derived NO may cause downregulation of IGF-I gene expression in hepatocytes. However, in cocultures, the iNOS inhibitor l-NIL prevented the effect of LPS on nitrite+nitrate levels, but only attenuated the LPS-induced decrease in IGF-I gene expression. We conclude that in hepatocytes, LPS-induced decrease in IGF-I is mainly due to induction of iNOS, whereas in the presence of Kupffer cells LPS inhibits IGF-I through NO release and through other inhibitory pathways.

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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 cells increased to 32.1% in TGF-β(A)-injected animals 48 h after injection. Furthermore, TGF-β(A)-injected rats did not survive 24 h after PH. Four hours after PH, 0.25 and 14.1% apoptotic hepatocytes were seen in Ctrl- and TGF-β(A)-injected rats, respectively. TGF-β(A)-induced apoptosis in primary rat hepatocytes was blocked with a pancaspase inhibitor. Thus autocrine expression of TGF-β(A) but not TGF-β(L) induces hepatocyte apoptosis in the normal rat liver. Rats overexpressing TGF-β(A) do not survive two-thirds PH due to hepatic apoptosis. Thus activation of TGF-β1 may be a critical step in the growth control of normal and proliferating rat hepatocytes.

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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 partial hepatectomy. Different liver cell populations and their receptor expression were characterized by two-color immunofluorescence and confocal laser scanning microscopy. Hepatocytes were detected by keratin K8 staining, and oval cells and bile ducts were recognized by keratin K19 expression. Enzyme-altered preneoplastic lesions ere identified by expression of placental glutathione S-transferase (GST-pi). Staining for these cellular markers was combined with immunodetection of EGFr and Met. Normal liver exhibited strong staining for EGFr in hepatocytes, whereas blood vessels, bile ducts, and some sinusoidal cells were Met-positive. In carcinogen-treated livers, oval cells showed Met but not EGFr immunostaining. GST-pi-positive foci displayed EGFr immunostaining at a similar intensity as surrounding hepatocytes, whereas Met was not detected. Our data indicate that putative liver cells (oval cells) have a growth receptor phenotype similar to that of bile ducts, whereas preneoplastic live lesions appear hepatocyte-like. These results indicate that the preferential proliferation of preneoplastic liver lesions compared to surrounding hepatocytes is not associated with an altered EGFr or Met phenotype.

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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 embryonic hepatogenesis. Although successful derivation of hepatocytes has been achieved through these protocols, the efficiency is not always ideal. Herein, we have tested several combinations of published protocols, for example, growth factor vs. small molecule and different time durations of treatment for definitive endoderm (DE) induction and further hepatocyte differentiation to develop an efficient DE induction and hepatocyte differentiation in a highly reproducible manner based on the stage-specific marker expression and functional analysis.

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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-treated hepatocytes without BV. BV suppressed TGF-β1-induced activation of the bcl-2 family and caspase family of proteins, which resulted in inhibition of poly ADP-ribose polymerase (PARP) cleavage. Furthermore, BV is not cytotoxic in the low concentrations used in this study. Low concentrations of BV potently suppress the apoptotic response in TGF-β1-treated hepatocytes; therefore, BV may have therapeutic potential for the treatment of liver diseases.

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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 hepatocytes positive for HGFA, which showed evidence of cell–cell heterogeneity in staining intensity. Immunoelectron microscopy detected ubiquitous distribution of the gold particle reaction product for HGFA in the cytoplasm of these hepatocytes, especially in the rough endoplasmic reticulum. Developmental analysis indicated that there was hardly any staining of HGFA until postnatal day 0 and that noticeable staining was initially detected in the pericentral hepatocytes on postnatal day 3. Subsequently, immunoreactivity increased and the distinct staining pattern had been established by postnatal day 30. These results suggest that HGFA proteins are produced in the hepatocytes surrounding the efferent hepatic veins in the mouse and that development of the unique distributing pattern takes place postnatally.

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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 hepatocytes. In addition, physiological concentrations of vasopressin cause a synergistic stimulation of [3H]thymidine uptake in rat liver cells in the presence of HGF.

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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 inhibited the TGF alpha-induced hepatocyte DNA synthesis, and this effect was specifically due to the inhibition of prostaglandin formation. Indomethacin also inhibited a TGF-alpha-induced increase in hepatocyte c-myc expression, indicating that prostaglandins mediate this increase, as previously shown for EGF. TGF alpha increased the expression of the EGF receptor gene, and this was prevented by the presence of an antibody against TGF alpha in the culture medium. We therefore suggest that TGF alpha induces hepatocyte proliferation either through coupling with its receptor (i.e. the EGF receptor) or by subsequent phosphorylation of lipocortin I. This leads to activation of phospholipase. A2, which seems to regulate the metabolism of arachidonic acid and the formation of prostaglandins. Thus hepatocyte proliferation in vitro appears to be controlled by a self-regulatory autocrine pathway involving activation of phospholipase A2 and secretion of prostaglandins and TGF alpha.

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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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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 hepatocytes and was efficient (2 to 20% of the cells). The patterns and absolute levels of reporter gene expression depended on assay conditions employed (plasmid concentration [optimal at 2.4 micrograms of DNA per ml] and duration of exposure [optimal between 5 and 10 h]), culture growth cycle stages (lag, log, or stationary phase), properties and tissue specificity of the promoter(s) tested, and composition (and timing of fluid change) of the culture medium with or without the hepatocyte mitogen human transforming growth factor-alpha. Initial observations suggest that during hepatocellular growth transitions, human transforming growth factor-alpha differentially regulates exogenously introduced promoters associated with hepatocyte-specific function and proliferation. These findings provide a simple, fast, and powerful approach to analyzing the molecular and cellular biology of hepatocyte growth control.

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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 hepatocytes and was efficient (2 to 20% of the cells). The patterns and absolute levels of reporter gene expression depended on assay conditions employed (plasmid concentration [optimal at 2.4 micrograms of DNA per ml] and duration of exposure [optimal between 5 and 10 h]), culture growth cycle stages (lag, log, or stationary phase), properties and tissue specificity of the promoter(s) tested, and composition (and timing of fluid change) of the culture medium with or without the hepatocyte mitogen human transforming growth factor-alpha. Initial observations suggest that during hepatocellular growth transitions, human transforming growth factor-alpha differentially regulates exogenously introduced promoters associated with hepatocyte-specific function and proliferation. These findings provide a simple, fast, and powerful approach to analyzing the molecular and cellular biology of hepatocyte growth control.

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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 temporally restricted model of hepatic repair in which large-scale hepatocyte injury and regeneration are initiated through the acute loss of Mdm2 in hepatocytes, resulting in the rapid, coordinated proliferation of BECs. We found that transient, early activation of Notch1- and Notch3-mediated signaling and entrance into the cell cycle preceded the phenotypic expansion of BECs into hepatocytes. Notch inhibition reduced BEC proliferation, which resulted in failure of BECs to differentiate into hepatocytes, indicating that Notch-dependent expansion of BECs is essential for hepatocyte regeneration. Notch signaling increased the abundance of the insulin-like growth factor 1 receptor (IGF1R) in BECs, and activating IGFR signaling increased BEC numbers but suppressed BEC differentiation into hepatocytes. These results suggest that different signaling mechanisms control BEC expansion and hepatocyte differentiation.

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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 medium, and exposed to insulin (Ins, 10−6 M), glucagon (Glu, 10−6 M), triiodothyronine (T3, 10−7 M), dexamethasone (Dex, 10−6 M) and glucagon-like peptide (GLP, 10−6 M), in the presence and absence of GH (5×10−9 M). GH always increased IGF-I mRNA. None of the other hormones tested alone affected IGF-I mRNA. However, Dex, Ins and Glu reduced the response to GH. The response to GH was inhibited by Dex at concentrations of 10−12 M and above, by Ins at 10−9 M and above, and by Glu only at 10−6 M. Inhibition of GH response by glucocorticoids is found in other vertebrates. Salmon hepatocytes were very sensitive to Dex, suggesting that glucocorticoids may play an important role in salmon growth regulation even in unstressed conditions. Inhibition of GH response by Ins is the opposite of what is found in mammals and chickens, suggesting that the role of Ins in growth regulation may differ between fishes and tetrapods. To examine mechanisms for modulation of GH sensitivity, we measured hepatocyte GH receptor (GHR) mRNA levels. Ins inhibited and Dex stimulated GHR mRNA, suggesting that different mechanisms mediate the inhibition of GH response by these hormones. This study shows that glucocorticoids, Ins, and Glu induce GH resistance in cultured salmon hepatocytes.

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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, GRO-beta, GRO-gamma, epithelial neutrophil activating peptide-78 (ENA-78), and RANTES] and the cytokines tumor necrosis factor-alpha (TNF-alpha) and macrophage colony stimulating factor was upregulated in human hepatocytes after stimulation with IL-1 alpha or TNF-alpha or bacterial invasion. In contrast, expression of hematopoietic/ lymphoid growth factors by the same cells was either down-regulated (erythropoietin and stem cell factor) or unchanged (IL-7 and IL-15) in response to the identical stimuli. Hepatocytes did not express cytokines that often are associated with the regulation of antigen-specific immune responses (IL-2, IL-4, IL-5, IL-10, IL-12p40, IL-13, and interferon-gamma) or genes for several other proinflammatory cytokines [IL-1 alpha, IL-6, monocyte chemotactic protein-1 (MCP-1), and MCP-3] or hematopoietic growth factors (granulocyte colony stimulating factor, granulocyte macrophage colony stimulating factor, IL-3, and IL-11). Together, these studies suggest that hepatocytes can both initiate and amplify acute inflammatory responses in the liver through the regulated expression and secretion of a specific array of proinflammatory cytokines.

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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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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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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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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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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 transiently increased in livers during the progression of cholestatic hepatitis. When c-Met tyrosine phosphorylation was blocked in the livers of BDL-treated mice by anti-HGF IgG, hepatic dysfunction became evident, associated with the acceleration of hepatocyte necrosis and apoptosis. Inversely, administration of recombinant HGF into the mice led to the prevention of cholestasis-induced inflammation: HGF suppressed the hepatic expression of intracellular adhesion molecule-1 and neutrophil infiltration in BDL-treated mice. As a result, parenchymal necrosis was suppressed in the HGF-injected BDL mice. In addition, HGF supplement therapy reduced the number of apoptotic hepatocytes in cholestatic mice, associated with the early induction of Bcl-xL. The administration of HGF enhanced hepatic repair, via accelerating G1/S progression in hepatocytes. Our study showed that 1) upregulation of HGF production is required for protective mechanisms against cholestatic hepatitis and 2) enhancement of the intrinsic defense system by adding HGF may be a reasonable strategy to attenuate hepatic inflammation, necrosis, and apoptosis under bile-congestive conditions.

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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 of multiple myeloma and also under the experimental condition of hepatic transplantation is discussed.

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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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KANEKO, A. "Activation of Na+/H+ exchanger by hepatocyte growth factor in hepatocytes*1." Hepatology 22, no. 2 (1995): 629–36. http://dx.doi.org/10.1016/0270-9139(95)90589-8.

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Ikejima, K., S. Watanabe, T. Kitamura, M. Hirose, A. Miyazaki, and N. Sato. "Hepatocyte Growth Factor Inhibits Intercellular Communication via Gap Junctions in Rat Hepatocytes." Biochemical and Biophysical Research Communications 214, no. 2 (1995): 440–46. http://dx.doi.org/10.1006/bbrc.1995.2306.

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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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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 factors (PDGFs), vascular endothelial growth factor (VEGF), and TGF-β. TGF-β, a super-family of cytokines, creates tumor microenvironment by interacting through other growth factors (epidermal growth factor receptor (EGFR), PDGF, fibroblast growth factor (FGF), hepatocyte growth factor (HGF), VEGF), cytokines and chemokines, and extracellular matrix (ECM) remodeling. Hence, the HCC tumor microenvironment may now be recognized as an important participant of tumor progression to act as potential target to systemic therapies compared to targeted therapies.

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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 elevated. Serum levels of triglycerides, cholesterol, total protein, and albumin were also dose dependently increased, whereas alkaline phosphatase was reduced. From these data we conclude 1) that combining HGF/SF with dextran sulfate provides a novel method for delivering HGF/SF in a continuous manner, 2) that HGF/SF can induce liver growth in an intact animal, and 3) that HGF/SF-induced liver enlargement is associated with changes in serum biochemistry.

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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 devices will also result in enhanced phenotype and function. To test this hypothesis, we fabricated devices with small and large volumes. Both types of devices included a microstructured floor containing arrays of pyramidal wells to promote assembly of hepatocytes into spheroids with individual diameters of ~100 µm. The hepatocyte spheroids were found to be more functional, as evidenced by higher level of albumin synthesis, bile acid production, and hepatic enzyme expression, in low-volume compared with large-volume devices. Importantly, high functionality of spheroid cultures correlated with elevated levels of HGF secretion. Although decay of hepatic function (albumin secretion) was observed over the course 3 wk, this behavior could be abrogated by inhibiting TGF-β1 signaling. With TGF-β1 inhibitor, microfluidic hepatocyte spheroid cultures maintained high and stable levels of albumin synthesis over the course of 4 wk. To further highlight utility of this culture platform for liver disease modeling, we carried out alcohol injury experiments in microfluidic devices and tested protective effects of interleukin-22: a potential therapy for alcoholic hepatitis.

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Ashizawa, Tatsuto, Tatsuya Aoki, Tetsuo Sumi, et al. "The Study of Hepatocyte Growth Factor (HGF) in the Spreading of Colorectal Cancer." Japanese Journal of Gastroenterological Surgery 35, no. 5 (2002): 480–86. http://dx.doi.org/10.5833/jjgs.35.480.

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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 were treated or not with HGF, reactive oxygen species present in cholesterol overloaded hepatocytes significantly decreased, and this effect was particularly associated with the increase in glutathione and related enzymes, such asγ-gamma glutamyl cysteine synthetase, GSH peroxidase, and GSH-S-transferase. Our data clearly indicate that HGF displays an antioxidant response by inducing the glutathione-related protection system.

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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 enhanced activities of epidermal growth factor receptor and STAT5A, reduced activities of cMet and p70S6K, decreased production of IL-6, TNFα, and hepatocyte growth factor, suppressed cyclin D1 expression, increased cyclin A1 expression, and early activated cyclin A2 expression. As a result, pregnancy allowed the remnant hepatocytes to enter the cell cycle at least 12 h earlier, increased hepatic fat accumulation, and enhanced hepatocyte mitosis. Consequently, pregnancy ameliorated maternal liver regeneration following PH. In addition, a report showed that maternal liver regrowth after PH is driven mainly by hepatocyte hypertrophy rather than hyperplasia during the second half of gestation in young adult mice. In contrast, we demonstrate that maternal liver relies mainly on hepatocyte hyperplasia instead of hypertrophy to restore the lost mass after PH. Overall, we demonstrate that pregnancy facilitates maternal liver regeneration likely via triggering an early onset of hepatocyte replication, accumulating excessive liver fat, and promoting hepatocyte mitosis. The results from our current studies enable us to gain more insights into how maternal liver regeneration progresses during gestation. NEW & NOTEWORTHY We demonstrate that pregnancy may generate positive effects on maternal liver regeneration following partial hepatectomy, which are manifested by early entry of the cell cycle of remnant hepatocytes, increased hepatic fat accumulation, enhanced hepatocyte mitosis, and overall accelerated liver regrowth.

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Won, Jong-Ho, Dong-Ho Choi, Jung-Hoon Kim, et al. "Human Mesenchymal Stem Cells Injected Via Portal Vein Are Differentiated into Human Hepatocytes in Regenerating Rat Liver." Blood 106, no. 11 (2005): 1694. http://dx.doi.org/10.1182/blood.v106.11.1694.1694.

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Abstract Objectives: Human mesenchymal stem cells (MSCs) possess versatile differentiation potential ranging from mesenchyme-related multipotency to neuroectodermal and endodermal competency. Evidence has been accumulated to indicate that certain compartments of bone marrow cells are capable to differentiating into hepatocytes in vitro. In this study we attempted to examine the differentiation ability of human MSCs into hepatocytes in vitro and in vivo by injected them into rat portal vein in partially resected rat liver model. Materials and Methods: MSCs were isolated from human bone marrow and induced differentiation with our protocol containing hepatocyte growth factor in vitro. Four - to - 5 week-old female Sprague Dawley rats were used for xenotransplantation model. Culture expanded MSCs (5 X 106 cells/rat) were injected into the portal vein and 70% hepatectomy was performed on the subsequent day. All rats were immunosuppressed with a daily intraperitoneal injection of cyclosporine A. Results: The morphology of the MSCs was changed into hepatocyte-like cells after in vitro culture for 28days and expression of hepatocyte specific genes also confirmed with RT-PCR and immunohistochemical stain. Transplanted MSCs differentiated into hepatocytes and they surprisingly composed hepatic cords with expression of the human albumin and human hepatocyte specific genes at 21 days after infusion. Conclusion: We have demonstrated that human MSCs can differentiate into functional hepatocyte-like cells in vitro and in vivo. Therefore, human MSCs may become an alternative source to hepatocyte regeneration or liver cell transplantation.

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TSUBOUCHI, HIROHITO. "Hepatocyte growth factor (HGF)." Kanzo 39, no. 7 (1998): 413–27. http://dx.doi.org/10.2957/kanzo.39.413.

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Nowatari, Takeshi, Kiyoshi Fukunaga, and Nobuhiro Ohkohchi. "Regulation of Signal Transduction and Role of Platelets in Liver Regeneration." International Journal of Hepatology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/542479.

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Among all organs, the liver has a unique regeneration capability after sustaining injury or the loss of tissue that occurs mainly due to mitosis in the hepatocytes that are quiescent under normal conditions. Liver regeneration is induced through a cascade of various cytokines and growth factors, such as, tumor necrosis factor alpha, interleukin-6, hepatocyte growth factor, and insulin-like growth factor, which activate nuclear factorκB, signal transducer and activator of transcription 3, and phosphatidyl inositol 3-kinase signaling pathways. We previously reported that platelets can play important roles in liver regeneration through a direct effect on hepatocytes and collaborative effects with the nonparenchymal cells of the liver, including Kupffer cells and liver sinusoidal endothelial cells, which participate in liver regeneration through the production of various growth factors and cytokines. In this paper, the roles of platelets and nonparenchymal cells in liver regeneration, including the associated cytokines, growth factors, and signaling pathways, are described.

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Journal articles on the topic 'Hepatocyte growth facter'

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