scholarly journals Involvement of hepatocyte growth factor in increased integrin expression on HepG2 cells triggered by adhesion to endothelial cells

1997 ◽  
Vol 75 (1) ◽  
pp. 47-53 ◽  
Author(s):  
N Kawakami-Kimura ◽  
T Narita ◽  
K Ohmori ◽  
T Yoneda ◽  
K Matsumoto ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hepg2 Cells ◽  
Integrin Expression ◽  
Hepatocyte Growth

Hepatocyte growth factor suppresses the anticancer effect of irinotecan by decreasing the level of active metabolite in HepG2 cells

2011 ◽  
Vol 82 (11) ◽  
pp. 1720-1730 ◽  
Author(s):  
Manabu Okumura ◽  
Tomomi Iwakiri ◽  
Akinori Takagi ◽  
Yasutoshi Hirabara ◽  
Yohei Kawano ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hepg2 Cells ◽  
Active Metabolite ◽  
Anticancer Effect ◽  
Hepatocyte Growth

scholarly journals Enhancement of Hepatocyte Growth Factor-Induced Cell Scattering in N-Acetylglucosaminyltransferase III-transfected HepG2 Cells

2004 ◽  
Vol 27 (6) ◽  
pp. 781-785 ◽  
Author(s):  
Masashi Hyuga ◽  
Sumiko Hyuga ◽  
Nana Kawasaki ◽  
Miyako Ohta ◽  
Satsuki Itoh ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hepg2 Cells ◽  
Cell Scattering ◽  
Hepatocyte Growth

Expression of hepatocyte growth factor activator inhibitor type 1 in endothelial cells

Human Cell ◽  
2006 ◽  
Vol 19 (3) ◽  
pp. 91-97 ◽  
Author(s):  
Yutaka Akiyama ◽  
Miyuki Nagai ◽  
Wataru Komaki ◽  
Kousuke Marutsuka ◽  
Yujiro Asada ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hepatocyte Growth Factor Activator ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
Hepatocyte Growth ◽  
Activator Inhibitor

Hepatocyte growth factor induces an endothelin-mediated decline in glomerular filtration rate

2005 ◽  
Vol 288 (1) ◽  
pp. F8-F15 ◽  
Author(s):  
Purba Biswas ◽  
Abinash Roy ◽  
Rujun Gong ◽  
Angelito Yango ◽  
Evelyn Tolbert ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Glomerular Filtration Rate ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Initial Increase ◽  
Dependent Manner ◽  
Hemodynamic Changes ◽  
Hepatocyte Growth

Hepatocyte growth factor (HGF) is a multifunctional cytokine that plays a crucial role in renal development, injury, and repair. HGF also serves a protective role in chronic renal disease by preventing tissue fibrosis. Endothelin-1 (ET-1), produced primarily by endothelial cells, is a potent vasoconstrictor that also acts as a proinflammatory peptide, promoting vascular injury and renal damage. In addition to mediating a variety of epithelial cell responses, HGF also induces hemodynamic changes that are poorly understood. The aim of the present study was to study the acute and chronic effects of HGF on ET-1 production in the kidney. We hypothesized that hemodynamic changes upon HGF treatment are likely mediated by immediate ET-1 release, whereas protection from renal fibrosis in rats chronically treated with HGF is likely due to suppression of ET-1 production. Acute HGF infusion into rats caused a decline in blood pressure that was enhanced by pretreatment with bosentan (an endothelin A and B receptor antagonist). HGF infusion also resulted in a decline in glomerular filtration rate (GFR) that could be entirely prevented by bosentan, suggesting that HGF acutely increases production and/or release of ET-1, which then mediates the observed decline in GFR. In cultured glomerular endothelial cells, HGF induced ET-1 production in a dose-dependent manner. Moreover, although there was an initial increase in ET-1 production upon HGF treatment, longer administration suppressed ET-1 production. This finding was consistent with the observation in vivo of a decrease in ET-1 production in renal parenchyma of rats chronically treated with HGF. Our data suggest both a hemodynamic and biological role for HGF-mediated ET-1 regulation.

scholarly journals Monocyte activation state regulates monocyte-induced endothelial proliferation through Met signaling

Blood ◽  
2010 ◽  
Vol 115 (16) ◽  
pp. 3407-3412 ◽  
Author(s):  
Shai Y. Schubert ◽  
Alejandro Benarroch ◽  
Juan Monter-Solans ◽  
Elazer R. Edelman
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Direct Interaction ◽  
Endothelial Cell Proliferation ◽  
Specific Cell ◽  
Mrna Levels ◽  
Hepatocyte Growth

Abstract Direct interaction of unactivated primary monocytes with endothelial cells induces a mitogenic effect in subconfluent, injured endothelial monolayers through activation of endothelial Met. We now report that monocytes' contact-dependent mitogenicity is controlled by activation-mediated regulation of hepatocyte growth factor. Direct interaction of unactivated monocytes with subconfluent endothelial cells for 12 hours resulted in 9- and 120-fold increase in monocyte tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β) mRNA levels and bitemporal spike in hepatocyte growth factor that closely correlates with endothelial Met and extracellular signal-related kinase (ERK) phosphorylation. Once activated, monocytes cannot induce a second wave of endothelial cell proliferation and endothelial Met phosphorylation and soluble hepatocyte growth factor levels fall off. Monocyte-induced proliferation is dose dependent and limited to the induction of a single cell cycle. Monocytes retain their ability to activate other endothelial cells for up to 8 hours after initial interaction, after which they are committed to the specific cell. There is therefore a profoundly sophisticated mode of vascular repair. Confluent endothelial cells ensure vascular quiescence, whereas subconfluence promotes vessel activation. Simultaneously, circulating monocytes stimulate endothelial cell proliferation, but lose this potential once activated. Such a system provides for the fine balance that can restore vascular and endothelial homeostasis with minimal overcompensation.

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