scholarly journals Relationship of Keratinocyte Growth Factor and Hepatocyte Growth Factor Levels in Rat Lung Lavage Fluid to Epithelial Cell Regeneration after Bleomycin

1999 ◽  
Vol 155 (3) ◽  
pp. 949-954 ◽  
Author(s):  
Ian Y.R. Adamson ◽  
Julita Bakowska
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Hepatocyte Growth Factor ◽  
Keratinocyte Growth Factor ◽  
Lavage Fluid ◽  
Lung Lavage ◽  
Cell Regeneration ◽  
Rat Lung ◽  
Relationship Of ◽  
Hepatocyte Growth

Epithelial cell spreading induced by hepatocyte growth factor influences paxillin protein synthesis and posttranslational modification

2004 ◽  
Vol 287 (4) ◽  
pp. G886-G898 ◽  
Author(s):  
Ann M. Hopkins ◽  
Matthias Bruewer ◽  
G. Thomas Brown ◽  
A’Drian A. Pineda ◽  
Julie J. Ha ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Hepatocyte Growth Factor ◽  
Fluorescent Protein ◽  
Kinase Inhibitor ◽  
Dominant Negative ◽  
Dependent Manner ◽  
Epithelial Migration ◽  
Cell Matrix ◽  
Hepatocyte Growth

Superficial wounds in the gastrointestinal tract rapidly reseal by coordinated epithelial cell migration facilitated by cytokines such as hepatocyte growth factor (HGF)/scatter factor released in the wound vicinity. However, the mechanisms by which HGF promotes physiological and pathophysiologic epithelial migration are incompletely understood. Using in vitro models of polarized T84 and Caco-2 intestinal epithelia, we report that HGF promoted epithelial spreading and RhoA GTPase activation in a time-dependent manner. Inducible expression of enhanced green fluorescent protein-tagged dominant-negative RhoA significantly attenuated HGF-induced spreading. HGF expanded a zone of partially flattened cells behind the wound edge containing basal F-actin fibers aligned in the direction of spreading. Concomitantly, plaques positive for the focal adhesion protein paxillin were enhanced. HGF induced an increase in the translation of paxillin and, to a lesser extent, β1-integrin. This was independent of cell-matrix adhesion through β1-integrin. Subcellular fractionation revealed increased cosedimentation of paxillin with plasma membrane-containing fractions following HGF stimulation, without corresponding enhancements in paxillin coassociation with β1 integrin or actin. Tyrosine phosphorylation of paxillin was reduced by HGF and was sensitive to the Src kinase inhibitor PP2. With these taken together, we propose that HGF upregulates a free cytosolic pool of paxillin that is unaffiliated with either the cytoskeleton or focal cell-matrix contacts. Thus early spreading responses to HGF may partly relate to increased paxillin availability for incorporation into, and turnover within, dynamic cytoskeletal/membrane complexes whose rapid and transient adhesion to the matrix drives migration.

scholarly journals EVALUATION OF SALIVARY HEPATOCYTE GROWTH FACTOR LEVELS IN CHRONIC PERIODONTITIS PATIENTS BEFORE AND AFTER NON-SURGICAL PERIODONTAL TREATMENT

2020 ◽  
pp. 8-10
Author(s):  
Madhavi T ◽  
Mathew John ◽  
Bindu Rachel Thomas ◽  
Sabari Chandramohan ◽  
Aswathy S ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Chronic Periodontitis ◽  
Periodontal Treatment ◽  
Periodontal Tissues ◽  
Whole Saliva ◽  
Before And After ◽  
Unstimulated Whole Saliva ◽  
Relationship Of ◽  
Hepatocyte Growth

Hepatocyte Growth Factor (HGF) or Scatter Factor (SF) is a growth factor which restrains the reconstruction of profound periodontal tissues. The study estimated the salivary HGF levels in unstimulated whole saliva in chronic periodontitis patients prior to treatment and also at 2nd and 6th week after non-surgical periodontal treatment and also aimed to determine the relationship of salivary HGF levels with the clinical periodontal parameters. This was a prospective-analytical study which included 45 subjects with chronic periodontitis. The highest mean concentration of HGF was obtained at the baseline and the lowest mean HGF concentration was obtained at the 6th week. There was significant decrease in the salivary HGF levels among the patients subsequent to scaling and root planing. Moreover the salivary HGF levels indicated a positive correlation with the clinical parameters at the sixth week. The above results propose that salivary HGF levels could be utilized as a biomarker for checking the response to periodontal treatment in chronic periodontitis patients.

scholarly journals In Vivo Gene Transfection With Hepatocyte Growth Factor via the Pulmonary Artery Induces Angiogenesis in the Rat Lung

Circulation ◽  
2002 ◽  
Vol 106 (12_suppl_1) ◽  
Author(s):  
Masamichi Ono ◽  
Yoshiki Sawa ◽  
Kunio Matsumoto ◽  
Toshikazu Nakamura ◽  
Yasufumi Kaneda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Growth Factor ◽  
Gene Transfer ◽  
Pulmonary Artery ◽  
Hepatocyte Growth Factor ◽  
Left Lung ◽  
Blood Perfusion ◽  
Capillary Density ◽  
Rat Lung ◽  
Hepatocyte Growth

Background Recent studies have demonstrated that gene transfer with hepatocyte growth factor (HGF) induces angiogenesis for coronary and peripheral artery diseases. We investigated the ability of gene transfer with human HGF to induce angiogenesis in the rat lung. Methods and Results The left lung was selectively transfected with a cDNA encoding human HGF via the left pulmonary artery, using the HVJ-liposome method (H group); rats transfected with the same vector lacking the HGF gene served as controls (C group). HGF gene transfer significantly increased the capillary density in the left lung compared with the C group 7 days after transfection (15.0±1.3 versus 8.0±1.7 mm 2 , P <0.01). The left to right average blood perfusion ratio detected by laser Doppler imaging increased significantly in the H group 14 days after transfection (1.12±0.09 versus 0.91±0.11, P <0.01). A right pulmonary artery clamp test, in which only the left lung received all the pulmonary blood flow from the right ventricle, revealed that the increase in right ventricular pressure was significantly attenuated in the H group compared with the C group 7 days after transfection (8.6±3.5 versus 15.3±2.8 mm Hg, P <0.01). Conclusions Trans-pulmonary arterial transfer of the human HGF gene into the left lung increased capillary density and blood perfusion, and decreased vascular resistance when blood flow increased. These results suggest therapeutic angiogenesis induced by HGF gene expression in the lung may be found suitable in treating subjects with decreased pulmonary vasculature or increased pulmonary vascular resistance.

scholarly journals Autocrine Interactions of Keratinocyte Growth Factor, Hepatocyte Growth Factor, and Kit-Ligand in the Regulation of Normal Ovarian Surface Epithelial Cells*

Endocrinology ◽  
2000 ◽  
Vol 141 (7) ◽  
pp. 2532-2539 ◽  
Author(s):  
Jeff A. Parrott ◽  
Rachel Mosher ◽  
Grace Kim ◽  
Michael K. Skinner
Keyword(s):  
Ovarian Cancer ◽  
Growth Factors ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Keratinocyte Growth Factor ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Kit Ligand ◽  
Ovarian Surface ◽  
Hepatocyte Growth

Ovarian tumors are primarily derived from the layer of epithelium surrounding the ovary termed the ovarian surface epithelium (OSE). Although extensive research has focused on established ovarian tumors, relatively little is known about the normal biology of the OSE that gives rise to ovarian cancer. The local expression and actions of growth factors are likely involved in both normal and tumorigenic OSE biology. The current study investigates the expression and action of keratinocyte growth factor (KGF), hepatocyte growth factor (HGF), and kit-ligand (KL) in normal ovarian surface epithelium (OSE). The actions of various growth factors on KGF, HGF, and KL expression are examined. Observations indicate that freshly isolated normal OSE express the genes for KGF, HGF, and KL and expression is maintained in vitro. KGF messenger RNA expression in OSE was found to be stimulated by KGF and HGF, but not KL. HGF expression in OSE was found to be stimulated by KGF, HGF, and KL. KL expression in OSE was also found to be stimulated by KGF, HGF, and KL. Therefore, the various growth factors can regulate the mRNA expression of each other in OSE. Effects of growth factors on OSE growth were examined. KGF, HGF, and KL stimulated OSE growth to similar levels as the positive control epidermal growth factor. Observations suggest that KGF, HGF, and KL interact to promote OSE growth and growth factor expression. The ability of these growth factors to interact in a positive autocrine feedback loop is postulated to be important for normal OSE biology. Paracrine interactions with the adjacent stromal cells will also be a factor in OSE biology. Abnormal interactions of these growth factors may be involved in the onset and progression of ovarian cancer.

scholarly journals Activation of Cdc42, Rac, PAK, and Rho-Kinase in Response to Hepatocyte Growth Factor Differentially Regulates Epithelial Cell Colony Spreading and Dissociation

2000 ◽  
Vol 11 (5) ◽  
pp. 1709-1725 ◽  
Author(s):  
Isabelle Royal ◽  
Nathalie Lamarche-Vane ◽  
Louie Lamorte ◽  
Kozo Kaibuchi ◽  
Morag Park
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Hepatocyte Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Rho Kinase ◽  
Cell Spreading ◽  
Dominant Negative ◽  
Phosphatidylinositol 3 Kinase ◽  
Mesenchymal Transition ◽  
Hepatocyte Growth

Hepatocyte growth factor (HGF), the ligand for the Met receptor tyrosine kinase, is a potent modulator of epithelial–mesenchymal transition and dispersal of epithelial cells, processes that play crucial roles in tumor development, invasion, and metastasis. Little is known about the Met-dependent proximal signals that regulate these events. We show that HGF stimulation of epithelial cells leads to activation of the Rho GTPases, Cdc42 and Rac, concomitant with the formation of filopodia and lamellipodia. Notably, HGF-dependent activation of Rac but not Cdc42 is dependent on phosphatidylinositol 3-kinase. Moreover, HGF-induced lamellipodia formation and cell spreading require phosphatidylinositol 3-kinase and are inhibited by dominant negative Cdc42 or Rac. HGF induces activation of the Cdc42/Rac-regulated p21-activated kinase (PAK) and c-Jun N-terminal kinase, and translocation of Rac, PAK, and Rho-dependent Rho-kinase to membrane ruffles. Use of dominant negative and activated mutants reveals an essential role for PAK but not Rho-kinase in HGF-induced epithelial cell spreading, whereas Rho-kinase activity is required for the formation of focal adhesions and stress fibers in response to HGF. We conclude that PAK and Rho-kinase play opposing roles in epithelial–mesenchymal transition induced by HGF, and provide new insight regarding the role of Cdc42 in these events.

Sign in / Sign up

Export Citation Format

Share Document