scholarly journals Morphogenetic Mechanisms of Epithelial Tubulogenesis: MDCK Cell Polarity Is Transiently Rearranged without Loss of Cell–Cell Contact during Scatter Factor/Hepatocyte Growth Factor-Induced Tubulogenesis

1998 ◽  
Vol 204 (1) ◽  
pp. 64-79 ◽  
Author(s):  
Anne L. Pollack ◽  
Raymond B. Runyan ◽  
Keith E. Mostov
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Polarity ◽  
Mdck Cell ◽  
Cell Contact ◽  
Scatter Factor ◽  
Hepatocyte Growth ◽  
Cell Cell

scholarly journals Hepatocyte Growth Factor Alters Renal Epithelial Cell Susceptibility to Uropathogenic Escherichia coli

2001 ◽  
Vol 12 (12) ◽  
pp. 2543-2553
Author(s):  
John H. Wu ◽  
Barry J. Billings ◽  
Daniel F. Balkovetz
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Growth Factor ◽  
Epithelial Cell ◽  
Hepatocyte Growth Factor ◽  
Cell Polarity ◽  
Mdck Cell ◽  
Cell Monolayers ◽  
Hepatocyte Growth

ABSTRACT. The urinary tract is frequently the source of Escherichia coli bacteremia. Bacteria from the urinary tract must cross an epithelial layer to enter the bloodstream. Hepatocyte growth factor (HGF) alters the polarity of Madin-Darby canine kidney (MDCK) epithelial cells. The role of cell polarity in determining renal epithelial resistance to Escherichia coli invasion is not well known. A model of polarized and HGF-treated MDCK epithelial cells grown on filters was used to study the role of epithelial cell polarity during the interaction of nonvirulent (XL1-Blue) and uropathogenic (J96) strains of Escherichia coli with renal epithelium. Basolateral exposure of MDCK cells to J96, but not XL1-Blue, resulted in loss of transepithelial resistance (TER), which was due to epithelial cytotoxicity and not degradation of epithelial junctional proteins by bacterial proteases. Apical exposure to both J96 and XL1-Blue did not alter TER. Pretreatment of polarized MDCK cell monolayers with HGF renders the cells sensitive to loss of TER and cytotoxicity by apical exposure to J96. Analysis by confocal microscopy demonstrated that HGF treatment of MDCK cell monolayers also greatly enhances adherence of J96 to the apical surface of the cell monolayer. These data demonstrate that the basolateral surface of polarized epithelia is more susceptible to J96 cytotoxicity. The data also support the hypothesis that processes that alter epithelial cell polarity increase sensitivity of epithelia to bacterial injury and adherence from the apical compartment.

Modulation of scatter factor/hepatocyte growth factor activity by cell-substratum adhesion

1994 ◽  
Vol 107 (5) ◽  
pp. 1265-1275 ◽  
Author(s):  
P. Clark
Keyword(s):  
Cell Adhesion ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Separation ◽  
Prolonged Exposure ◽  
Collagen Gels ◽  
Scatter Factor ◽  
Tubule Formation ◽  
Hepatocyte Growth ◽  
Cell Cell

Scatter factor/hepatocyte growth factor (SF/HGF) is a multifunctional growth and motility factor whose activities vary with cell type. Here, the composition of the substratum was found to profoundly alter the scattering activities of SF/HGF, but not its mitogenetic effects, in MDCK cells. Whereas enhancement of DNA synthesis and induction of cell flattening by SF/HGF were independent of substratum composition (i.e. occurred on both fibronectin and vitronectin surfaces), colony dispersion as a result of cell separation fails to occur or is markedly reduced on surfaces where vitronectin is the major adhesive ligand. Prolonged exposure of non-scattering cultures to SF/HGF resulted in cells at colony margins producing long protrusions, which indicate that the motility of these cells is stimulated but ‘frustrated’ by the lack of breakdown of cell-cell adhesion. Scattering therefore appears to comprise two major components: increased motility and breakdown of cell-cell adhesion. The pathway leading to the breakdown of cell-cell contacts is modulated by downstream signals from extracellular matrix receptors. When cultured on immobilised fibronectin, vitronectin or a surface containing both, colony dissociation correlates with the presence of fibronectin, suggesting that positive signals from fibronectin receptors are required for SF/HGF-induced cell separation. Comparison of the findings in this study with those of a recent report on the modulation of SF/HGF-induced tubulogenesis by ECM (Santos, O. F. P. and Nigam, S. K. (1993) Dev. Biol. 160, 293–302), where vitronectin in type-1 collagen gels alters the pattern of SF/HGF-induced MDCK tubule formation from highly branched to long and unbranched, suggests that cell motility enhancement leads to tubule formation whereas the breakdown of cell-cell adhesion is required for tubule branching.

scholarly journals Characterization of the Scatter Factor/Hepatocyte Growth Factor Gene Promoter

1995 ◽  
Vol 270 (2) ◽  
pp. 830-836 ◽  
Author(s):  
Antje Plaschke-Schlütter ◽  
Jürgen Behrens ◽  
Ermanno Gherardi ◽  
Walter Birchmeier
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Gene Promoter ◽  
Scatter Factor ◽  
Factor Gene ◽  
Growth Factor Gene ◽  
Hepatocyte Growth

scholarly journals Paracrine Regulation of Germinal Center B Cell Adhesion through the c-Met–Hepatocyte Growth Factor/Scatter Factor Pathway

1997 ◽  
Vol 185 (12) ◽  
pp. 2121-2131 ◽  
Author(s):  
Robbert van der Voort ◽  
Taher E.I. Taher ◽  
Robert M.J. Keehnen ◽  
Lia Smit ◽  
Martijn Groenink ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
T Cell ◽  
B Cells ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Tyrosine Kinase ◽  
B Cell ◽  
Germinal Center ◽  
Scatter Factor ◽  
Hepatocyte Growth

T cell–dependent humoral immune responses are initiated by the activation of naive B cells in the T cell areas of the secondary lymphoid tissues. This primary B cell activation leads to migration of germinal center (GC) cell precursors into B cell follicles where they engage follicular dendritic cells (FDC) and T cells, and differentiate into memory B cells or plasma cells. Both B cell migration and interaction with FDC critically depend on integrin-mediated adhesion. To date, the physiological regulators of this adhesion were unkown. In the present report, we have identified the c-met–encoded receptor tyrosine kinase and its ligand, the growth and motility factor hepatocyte growth factor/scatter factor (HGF/SF), as a novel paracrine signaling pathway regulating B cell adhesion. We observed that c-Met is predominantly expressed on CD38+CD77+ tonsillar B cells localized in the dark zone of the GC (centroblasts). On tonsil B cells, ligation of CD40 by CD40-ligand, induces a transient strong upregulation of expression of the c-Met tyrosine kinase. Stimulation of c-Met with HGF/SF leads to receptor phosphorylation and, in addition, to enhanced integrin-mediated adhesion of B cells to both VCAM-1 and fibronectin. Importantly, the c-Met ligand HGF/SF is produced at high levels by tonsillar stromal cells thus providing signals for the regulation of adhesion and migration within the lymphoid microenvironment.

scholarly journals Normal and Malignant Prostate Epithelial Cells Differ in Their Response to Hepatocyte Growth Factor/Scatter Factor

2001 ◽  
Vol 159 (2) ◽  
pp. 579-590 ◽  
Author(s):  
Glenn A. Gmyrek ◽  
Marc Walburg ◽  
Craig P. Webb ◽  
Hsiao-Man Yu ◽  
Xueke You ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Hepatocyte Growth Factor ◽  
Scatter Factor ◽  
Prostate Epithelial Cells ◽  
Hepatocyte Growth ◽  
Malignant Prostate

Hepatocyte Growth Factor/Scatter Factor Stimulates Hair Growth of Mouse Vibrissae in Organ Culture

1994 ◽  
Vol 103 (3) ◽  
pp. 306-309 ◽  
Author(s):  
Toshimasa Jindo ◽  
Ryoji Tsuboi ◽  
Ryusuke Imai ◽  
Kenji Takamori ◽  
Jeffrey S Rubin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Organ Culture ◽  
Hepatocyte Growth Factor ◽  
Hair Growth ◽  
Scatter Factor ◽  
Hepatocyte Growth

Involvement of hepatocyte growth factor/scatter factor and Met receptor signaling in hair follicle morphogenesis and cycling

2000 ◽  
Vol 14 (2) ◽  
pp. 319-332 ◽  
Author(s):  
Gerd Lindner ◽  
Andreas Menrad ◽  
Ermanno Gherardi ◽  
Glenn Merlino ◽  
Pia Welker ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Hair Follicle ◽  
Receptor Signaling ◽  
Met Receptor ◽  
Scatter Factor ◽  
Hepatocyte Growth

scholarly journals HGF Converts ErbB2/Neu Epithelial Morphogenesis to Cell Invasion

2005 ◽  
Vol 16 (2) ◽  
pp. 550-561 ◽  
Author(s):  
Hanane Khoury ◽  
Monica A. Naujokas ◽  
Dongmei Zuo ◽  
Veena Sangwan ◽  
Melanie M. Frigault ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Invasion ◽  
Single Cells ◽  
Epithelial Morphogenesis ◽  
Cell Junctions ◽  
Junction Protein ◽  
Hepatocyte Growth ◽  
E Cadherin ◽  
Cell Cell

Activation of the hepatocyte growth factor receptor Met induces a morphogenic response and stimulates the formation of branching tubules by Madin-Darby canine kidney (MDCK) epithelial cells in three-dimensional cultures. A constitutively activated ErbB2/Neu receptor, NeuNT, promotes a similar invasive morphogenic program in MDCK cells. Because both receptors are expressed in breast epithelia, are associated with poor prognosis, and hepatocyte growth factor (HGF) is expressed in stroma, we examined the consequence of cooperation between these signals. We show that HGF disrupts NeuNT-induced epithelial morphogenesis, stimulating the breakdown of cell-cell junctions, dispersal, and invasion of single cells. This correlates with a decrease in junctional proteins claudin-1 and E-cadherin, in addition to the internalization of the tight junction protein ZO-1. HGF-induced invasion of NT-expressing cells is abrogated by pretreatment with a pharmacological inhibitor of the mitogen-activated protein kinase kinase (MEK) pathway, which restores E-cadherin and ZO-1 at cell-cell junctions, establishing the involvement of MEK-dependent pathways in this process. These results demonstrate that physiological signals downstream from the HGF/Met receptor synergize with ErbB2/Neu to enhance the malignant phenotype, promoting the breakdown of cell-cell junctions and enhanced cell invasion. This is particularly important for cancers where ErbB2/Neu is overexpressed and HGF is a physiological growth factor found in the stroma.

Hepatocyte Growth Factor/Scatter Factor Promotes a Switch from E- to N-Cadherin in Chick Embryo Epiblast Cells

1999 ◽  
Vol 251 (1) ◽  
pp. 3-15 ◽  
Author(s):  
Steven M. DeLuca ◽  
Jacquelyn Gerhart ◽  
Eric Cochran ◽  
Eileen Simak ◽  
Jennifer Blitz ◽  
...  
Keyword(s):  
Growth Factor ◽  
Chick Embryo ◽  
Hepatocyte Growth Factor ◽  
Scatter Factor ◽  
Hepatocyte Growth
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