High efficacy of fibroblast and hepatocyte growth factors on the in vitro blastocyst production of post-thaw mouse two-cell embryo: The cryotop method

2011 ◽  
Vol 10 (69) ◽  
Author(s):  
Ghasemian
Keyword(s):  
Growth Factors ◽  
High Efficacy ◽  
Hepatocyte Growth Factors ◽  
Cell Embryo ◽  
Hepatocyte Growth

Gene expression of keratinocyte and hepatocyte growth factors during the healing of rat gastric mucosal lesions

1995 ◽  
Vol 109 (4) ◽  
pp. 1068-1077 ◽  
Author(s):  
Yoshikazu Kinoshita ◽  
Hirohisa Nakata ◽  
Sazzad Hassan ◽  
Masakyo Asahara ◽  
Chiharu Kawanami ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factors ◽  
Gastric Mucosal Lesions ◽  
Hepatocyte Growth Factors ◽  
Mucosal Lesions ◽  
Hepatocyte Growth

Mechanisms of recovery from mechanical injury of cultured rat hepatocytes

1996 ◽  
Vol 271 (3) ◽  
pp. C721-C727 ◽  
Author(s):  
H. T. Sponsel ◽  
P. S. Guzelian ◽  
S. E. Brown ◽  
R. Breckon ◽  
C. Ray ◽  
...  
Keyword(s):  
Growth Factors ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Primary Cultures ◽  
Rat Hepatocytes ◽  
Integrin Subunit ◽  
Hepatocyte Growth Factors ◽  
Beta 1 Integrin ◽  
Rate Of Recovery ◽  
Hepatocyte Growth

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.

Epidermal and hepatocyte growth factors stimulate chemotaxis in an intestinal epithelial cell line

1999 ◽  
Vol 277 (6) ◽  
pp. C1149-C1159 ◽  
Author(s):  
D. Brent Polk ◽  
Wei Tong
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Protein Kinase ◽  
Epithelial Cell ◽  
Intestinal Epithelial Cell ◽  
Intestinal Cells ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
Hepatocyte Growth Factors ◽  
Hepatocyte Growth

The migration of intestinal cells is important in the development and maintenance of normal epithelium, in a process that may be regulated by growth factors and cytokines. Although a number of growth factor receptors are expressed by intestinal cells, little progress has been made toward assignment of functional roles for these ligand-receptor systems. This study compares several growth factors and cytokines for their chemoattraction of the mouse small intestinal epithelial cell line. Epidermal and hepatocyte growth factors stimulated a rapid 30-fold chemotaxis of cells with delayed threefold migration toward transforming growth factor-β1. Despite stimulating proliferation, keratinocyte, fibroblast, or insulin-like growth factors did not stimulate directed migration. Chemotaxis required tyrosine kinase and phosphatidylinositol phospholipase C activities but not protein kinase C or mitogen-activated protein kinase activity. These findings suggest that the repertoire of growth factors capable of regulating directed intestinal epithelial cell migration is limited and that a divergence exists in the signal transduction pathways for directed vs. nondirected migration.

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