Interaction of Hepatocyte Growth Factor and Non-Steroidal Anti-Inflammatory Drugs during Gastric Epithelial Wound Healing

Vocal fold fibrotic scar is characterized by fibrosis of the lamina propria and epithelium, and is difficult to treat. Hepatocyte growth factor (HGF) has antifibrotic activity and has received attention as a possible therapeutic alternative to treat fibrosis. In this study, in order to clarify whether HGF can be involved in vocal fold scarring, we examined the existence of HGF and its receptor, c-Met, in rat vocal folds, and then the activity of HGF in rabbit injured vocal folds, using immunohistochemistry and enzyme-linked immunosorbent assay. We found HGF and c-Met on epithelial cells and gland cells of the rat vocal folds. On the injured vocal folds of rabbits, little HGF was observed immediately after injury, but prominent activity occurred simultaneously with reepithelialization of the vocal fold mucosa on days 10 to 15. The activity of HGF was observed on fibroblasts in the lamina propria, as well as the epithelium. It is suggested that HGF in the vocal folds is produced by the fibroblasts and delivered to the epithelium. The implication of these findings is that HGF is involved in wound healing of the vocal fold, and may provide an alternative approach in preventing and treating vocal fold scarring.

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Hepatocyte growth factor inhibits the formation of the basement membrane of alveolar epithelial cells in vitro

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00238.2002 ◽

2004 ◽

Vol 286 (5) ◽

pp. L939-L946 ◽

Cited By ~ 12

Author(s):

Akiko Furuyama ◽

Katsumi Mochitate

Keyword(s):

Wound Healing ◽

Growth Factor ◽

Epithelial Cells ◽

Basement Membrane ◽

Matrix Metalloproteinase ◽

Hepatocyte Growth Factor ◽

Collagen Fibrils ◽

Membrane Formation ◽

Hepatocyte Growth

Hepatocyte growth factor (HGF) is a pulmotrophic factor for the regeneration of injured pulmonary tissue. We investigated the role of HGF in basement membrane formation during wound healing by immortalized alveolar type II epithelial cells that could form a continuous basement membrane when they were cultured on collagen fibrils in the presence of entactin-contaminated laminin-1. Cells cultured with 5.0 ng/ml HGF neither formed a continuous basement membrane on collagen fibrils nor maintained a continuous basement membrane architecture on a basement membrane substratum. The cells showed increased secretion of matrix metalloproteinase-9 and urokinase-type plasminogen activator, and the HGF-induced inhibition of basement membrane formation was attenuated by addition of 200 ng/ml tissue inhibitor of matrix metalloproteinase-1. Cells sequentially exposed to HGF and 1.0 ng/ml transforming growth factor-β1 had enhanced basement membrane formation compared with those receiving these reagents in the reverse order or concurrently. HGF simultaneously stimulated proliferation and migration of the cells so that it advanced wound closure on the basement membrane substratum. The present results indicate that the role of HGF in wound healing is the stimulation of reepithelization, but this factor may also contribute to the degradation of the basement membrane.

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Suppression of lipopolysaccharide-induced corneal opacity by hepatocyte growth factor

Scientific Reports ◽

10.1038/s41598-021-04418-x ◽

2022 ◽

Vol 12 (1) ◽

Author(s):

Elsayed Elbasiony ◽

WonKyung Cho ◽

Sharad K. Mittal ◽

Sunil K. Chauhan

Keyword(s):

Growth Factor ◽

Hepatocyte Growth Factor ◽

Vision Loss ◽

Corneal Opacity ◽

Corneal Injury ◽

Immune Quiescence ◽

Epithelial Wound Healing ◽

Corneal Structure ◽

Hepatocyte Growth ◽

Treatment Of Infection

AbstractKeratitis induced by bacterial toxins, including lipopolysaccharide (LPS), is a major cause of corneal opacity and vision loss. Our previous study demonstrates hepatocyte growth factor (HGF) promotes epithelial wound healing following mechanical corneal injury. Here, we investigated whether HGF has the capacity to suppress infectious inflammatory corneal opacity using a new model of LPS-induced keratitis. Keratitis, induced by two intrastromal injections of LPS on day 1 and 4 in C57BL/6 mice, resulted in significant corneal opacity for up to day 10. Following keratitis induction, corneas were topically treated with 0.1% HGF or PBS thrice daily for 5 days. HGF-treated mice showed a significantly smaller area of corneal opacity compared to PBS-treated mice, thus improving corneal transparency. Moreover, HGF treatment resulted in suppression of α-SMA expression, compared to PBS treatment. HGF-treated corneas showed normalized corneal structure and reduced expression of pro-inflammatory cytokine, demonstrating that HGF restores corneal architecture and immune quiescence in corneas with LPS-induced keratitis. These findings offer novel insight into the potential application of HGF-based therapies for the prevention and treatment of infection-induced corneal opacity.

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