Hepatocyte growth factor/hepatopoietin A is expressed in fat-storing cells from rat liver but not myofibroblast-like cells derived from fat-storing cells

Schirmacher, Peter; Geerts, Albert; Pietrangelo, Antonello; Dienes, Hans Peter; Rogler, Charles E.

doi:10.1002/hep.1840150103

Cited by 199 publications

(102 citation statements)

References 27 publications

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“…HGF is expressed well in early cultures of activated primary HSC, although transition of HSC to ␣-SMA-expressing myofibroblast-like phenotype decreases HGF expression. 34 The need for physical disruption of the sinusoidal barrier should be commensurate with the induction of matrix degrading enzymes. During the initial phase of ischemic liver injury, Kupffer cell activation, phagocytic infiltration, and stimulation of sinusoidal endothelial cells, multiple soluble factors and cytokines with HSC-activating properties are released.…”

Section: Discussionmentioning

confidence: 99%

Hepatocyte transplantation activates hepatic stellate cells with beneficial modulation of cell engraftment in the rat

Benten¹,

Kumaran²,

Joseph³

et al. 2005

Hepatology

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Section: Discussionmentioning

confidence: 99%

Hepatocyte transplantation activates hepatic stellate cells with beneficial modulation of cell engraftment in the rat

Benten¹,

Kumaran²,

Joseph³

et al. 2005

Hepatology

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“…This interaction may occur via several mechanisms. Alison and colleagues 8 have speculated that Ito (or stellate) cells 42 may affect the oval cell response by 1) secreting metalloproteinases 43 specific for basement membrane proteins so that oval cells can invade damaged parenchyma; 2) secreting multiple growth factors [including hepatocyte growth factor 44,45 and transforming growth factor-␤ 39,46 ] to promote oval cell migration and differentiation; 3) creating a microenvironment featuring stromal components that resemble periportal regions, so that oval cells retain biliarylike properties early during regeneration; and 4) synthesizing and secreting laminin chains to stimulate endothelial invasion and sinusoid formation. 47 In addition, our observation that laminin fibers were associated with oval cells may be significant because adhesive interactions between cells and extracellular matrix molecules, including laminin, are proposed to be a critical *The oval cell response was classified by microscopic examination of paraformadehyde-fixed, paraffin-embedded sections stained with hematoxylin and eosin or anti-cytokeratin 19 antibody.…”

Section: Discussionmentioning

confidence: 99%

Hepatic Microenvironment Affects Oval Cell Localization in Albumin-Urokinase-Type Plasminogen Activator Transgenic Mice

Braun

Thompson

Sandgren

2003

The American Journal of Pathology

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Mice carrying an albumin-urokinase type plasminogen activator transgene (AL-uPA) develop liver disease secondary to uPA expression in hepatocytes. Transgene-expressing parenchyma is replaced gradually by clones of cells that have deleted transgene DNA and therefore are not subject to uPA-mediated damage. Diseased liver displays several abnormalities, including hepatocyte vacuolation and changes in nonparenchymal tissue. The latter includes increases in laminin protein within parenchyma and the appearance of cytokeratin 19-positive bile ductule-like cells (oval cells) both in portal regions and extending into the hepatic parenchyma. In this study, we subjected ALuPA mice to two-thirds partial hepatectomy to identify the response of these livers to additional growth stimulation. We observed several changes in hepatic morphology. First, the oval cells increased in number and often formed ductules in the parenchyma. Second, this cellular change was accompanied by a further increase in laminin associated with single or clusters of oval cells. Third, desmin-positive Ito cells increased in number and maintained close association with oval cells. Fourth, these changes were localized precisely to uPA-expressing areas of liver. Regenerating clones of uPA-deficient cells appeared to be unaffected both by stromal and cellular alterations. Thus, additional growth stimulation of diseased uPAexpressing liver induces an oval cell-like response, as observed in other models of severe hepatic injury, but the localization of this response seems to be highly regulated by the hepatic microenvironment.

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“…These consist of two chains linked together by disulphide bonds. Recent studies have suggested that HGF is produced by non-parenchymal hepatic cells including Kupffer cells (Noji et al, 1990), endothelial cells (Stoker et al, 1987;Shima et al, 1991), fibroblasts and fat-storing cells in the liver (Ramadori et al, 1992;Schirmacher et al, 1992), endothelial cells in the lung Yanagita et al, 1992). Experimentally, tumour cells are also known to produce HGF; HGF or mRNA encoding this factor has been detected in fibrosarcoma (Stoker et al, 1987), lung cancer (Yoshinaga et al, 1992;Rygaard et al, 1993;Tsao et al, 1993); hepatoma (Miyazaki et al, 1991) and pancreatic cancer cells (Hirota et al, 1993).…”

Section: Methodsmentioning

confidence: 99%

Serum hepatocyte growth factor as an index of disease status of patients with colorectal carcinoma

Fukuura

Miki²,

Inoue³

et al. 1998

Br J Cancer

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Summary To evaluate the clinical significance of serum levels of hepatocyte growth factor (HGF) in colorectal cancer patients, we measured the venous and portal concentrations of HGF in 60 patients. The tissue concentrations in the tumour and adjacent normal mucosa were also determined. The serum HGF concentration for the peripheral venous blood of the patients was significantly higher than that in normal controls. The content of HGF in cancer tissue was also significantly higher than that in normal mucosa, and it was correlated with the serum HGF concentration for the peripheral venous blood. The serum concentration of HGF reflected pathological features, including tumour size and lymph node or liver metastasis, and it showed an association with various preoperative nutritional parameters and the preoperative haemoglobin level. The serum HGF concentration was also correlated with the serum concentrations of immunosuppressive acidic protein and interleukin-6, indices of the host's immunological condition. Serum HGF seems to be a useful index of the disease status of patients with colorectal carcinoma.Keywords: hepatocyte growth factor; nutritional status; immunological status; colorectal cancer Hepatocyte growth factor (HGF) is a multifunctional cytokine that is the most potent known stimulator of hepatocyte growth and DNA synthesis Kaneko et al, 1992). HGF has also been recognized as a tumour-disseminating factor (Weidner et al, 1991;Mayer et al, 1993;Tannapfel et al, 1994). In several experimental studies, evidence has been acquired of a relation of HGF to the progression of tumour cells . Among the particularly important biological activities of HGF in tumour cells is its capacity to increase epithelial cell proliferation and motility (Gherardi et al, 1990). In clinical studies, a relationship between the concentration of HGF in serum or cancer tissue and the progression of disease has been noted in patients with gastric cancer (Taniguchi et al, 1997), oesophageal cancer (Takada et al, 1995) and breast cancer (Yamashita et al, 1994;Taniguchi et al, 1995). However, there are no reports regarding the clinical relevance of HGF in patients with colorectal carcinoma.Malnutrition or immunosuppression are involved in the development of life-threatening complications in patients with malignancies (Braga et al, 1988;Nishi et al, 1988;Dannhauser et al, 1995;Triantafillidis et al, 1995;Windsor et al, 1995;Goransson et al, 1996). Patients with advanced cancer and cachexia typically demonstrate modestly increased rates of energy expenditure with concomitant diminished food intake. These metabolic changes may be due to mediators released by the tumour or by the host (Keller, 1993). Recently, the role of cytokines in these metabolic changes was emphasized (Gambardella et al, 1997). In addition, the relationship between cytokines and an immunosuppressive substance has also been highlighted (Tanaka et al, 1993 The objective of this study was to evaluate the relationship between serum HGF concentration and clinicopathological ...

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Hepatocyte growth factor/hepatopoietin A is expressed in fat-storing cells from rat liver but not myofibroblast-like cells derived from fat-storing cells

Cited by 199 publications

References 27 publications

Hepatocyte transplantation activates hepatic stellate cells with beneficial modulation of cell engraftment in the rat

Hepatocyte transplantation activates hepatic stellate cells with beneficial modulation of cell engraftment in the rat

Hepatic Microenvironment Affects Oval Cell Localization in Albumin-Urokinase-Type Plasminogen Activator Transgenic Mice

Serum hepatocyte growth factor as an index of disease status of patients with colorectal carcinoma

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