Disease relevance of HGF

• Inhibition of HGF may be an appropriate therapeutic intervention in the case of persistent epithelial defects and to prevent fibrosis following a corneal stromal wound such as can occur after refractive surgery [1].
• We examined the role of the hepatocyte growth factor (HGF)/c-met system on invasion and metastasis of oral squamous cell carcinoma (SCC) cells [2].
• Albumin marks pseudopodia of astrocytoma cells responding to hepatocyte growth factor or serum [3].
• Expression and action of hepatocyte growth factor in human and bovine normal ovarian surface epithelium and ovarian cancer [4].
• The hepatocyte growth factor (HGF) has been crucially implicated in the development of proliferative retinal diseases; however, it is unclear whether retinal glial cells express or respond to HGF [5].

High impact information on HGF

• Hepatocyte growth factor regulates angiotensin converting enzyme expression [6].
• Hepatocyte growth factor releases epithelial and endothelial cells from growth arrest induced by transforming growth factor-beta1 [7].
• Molecular cloning and sequence analysis of the cDNA for a human serine protease reponsible for activation of hepatocyte growth factor. Structural similarity of the protease precursor to blood coagulation factor XII [8].
• PURPOSE: To investigate the effects of hepatocyte growth factor (HGF) and a small applied electric field (EF) on corneal epithelial cell (CEC) migration [9].
• Hepatocyte growth factor activates endothelial nitric oxide synthase by Ca(2+)- and phosphoinositide 3-kinase/Akt-dependent phosphorylation in aortic endothelial cells [10].

Biological context of HGF

• Sensitive quantitative RT-PCR assays were used to analyze gene expression of KGF, HGF, and KL in the ovary [11].
• The inhibition of granulosa cell steroid production by HGF is proposed to be the indirect effect of promoting cellular proliferation [12].
• PURPOSE: To investigate the effects of hepatocyte growth factor (HGF) and keratinocyte growth factor (KGF) on early wound healing in the corneal epithelium and stroma [1].
• BACKGROUND: Although hepatocyte growth factor (HGF) is also known as scatter factor, it induces epithelial morphogenesis in cultured bovine retinal pigment epithelial (RPE) cells [13].
• The 2.5-kbp HGF cDNA clone contained a 2190 bp open reading frame coding a 730 amino acid protein, while the 4.8-kbp c-Met cDNA clone contained a 4152 bp open reading frame coding a 1384 amino acid protein [14].

Anatomical context of HGF

• This study investigates the hypothesis that thecal cell-derived growth factors (e.g. KGF and HGF) regulate granulosa cell function, and granulosa cell-derived growth factors (e.g. KL) regulate thecal cell function [11].
• S1P-induced endothelial cell migration was maximum at 1 microM (approximately 8-fold increase with PA endothelium) and surpassed the maximal response evoked by either VEGF (10 ng/ml) (approximately 2.5-fold increase) or hepatocyte growth factor (HGF) (approximately 2.5-fold increase) [15].
• CONCLUSIONS: Treatment of RPE explants with HGF results in rapid disassembly of tight and adherens junctions associated with loss or redistribution of junctional proteins, decreased TER, and increased migration of RPE cells from the monolayer [16].
• Hormonal regulation of HGF was analyzed in hormone-treated theca cell cultures [12].
• In order to investigate the physiological role of HGF in the ovarian follicle, the developmental and hormonal regulation of HGF was examined during follicular development in the bovine ovary [12].

Associations of HGF with chemical compounds

• Steady-state levels of HGF mRNA in theca cells were increased by treatment with hCG (an LH agonist), but estradiol had no effect [12].
• In addition, HGF inhibited the ability of hCG to stimulate progesterone production by granulosa cells [12].
• The action of the LMW factor was not due to the actions of low molecular weight substances such as norepinephrine, estradiol, triiodothyronine, and putrescine, which enhance the action of EGF or HGF, since substantial amounts of these substances were not found in the extract [17].

Regulatory relationships of HGF

• Treatment with HGF reduced basal and FSH-stimulated levels of aromatase activity in bovine and rat granulosa cells [12].
• In fact, both EGF and TGF-beta1 induced significantly higher intakes of nuclear BrdU of the epithelial cells than HGF [18].
• CONCLUSION: Our results suggest that HGF promotes linkage of occludin to the cytoskeleton [13].

Other interactions of HGF

• Reverse transcription-polymerase chain reaction (RT-PCR) analysis was used to examine HGF expression in theca cells and the HGF receptor (HGFR or c-met) in granulosa cells [12].
• After 6 hours of treatment with HGF, occludin, claudin-1, and beta-catenin were redistributed from the membrane to the cytoplasm [16].
• KGF, HGF, and KL stimulated OSE growth to similar levels as the positive control epidermal growth factor [19].
• TGF-beta1-treated cells formed a more markedly thickened epithelial layer than HGF-treated cells [18].
• Hepatic HGF and IGFBP-5 mRNA levels did not differ between implanted and nonimplanted steers [20].

Analytical, diagnostic and therapeutic context of HGF

• This was in contrast to wounded organ cultures treated with 100 ng/mL HGF, in which large numbers of myofibroblasts were observed under the wound [1].
• HGF may become a therapeutic candidate in physiological recovery of RPE cells and in preparation of RPE monolayers for transplantation [13].
• Western blotting also showed that insoluble occludin was more abundant in HGF-treated cells [13].

References