Background/objectives: When the lamina propria of the vocal fold is replaced by fibrosis after wound healing, it is difficult to restore an appropriate viscoelasticity of the vocal fold. To treat fibrotic scarring, material that reduces collagen deposition and increases soft amorphous substances, such as hyaluronic acid, is required. The potential use of hepatocyte growth factor (HGF) is intriguing. In this study, the authors examined canine vocal fold fibroblasts to determine how HGF contributes to the production of extracellular matrix. More specifically, the authors describe how the productions of hyaluronic acid, collagen type I, and fibronectin are associated with administration of HGF and transforming growth factor beta1.
Study design: In vitro.
Methods: Fibroblasts were collected from the lamina propria of the vocal folds of five Beagles and were cultured with and without HGF or transforming growth factor beta1. The productions of hyaluronic acid, collagen type I, and fibronectin in supernatants culture were examined using ELISA.
Results: Hepatocyte growth factor stimulated hyaluronic acid production, reduced collagen type I production, and did not affect fibronectin production, while transforming growth factor beta1 stimulated the productions of all components.
Conclusions: Collagen type I appears to be a major contributor in creation of fibrosis, and excessive fibronectin may stiffen the tissue. Since HGF reduced collagen type I production from fibroblasts and increased hyaluronic acid, HGF is considered to have therapeutic potential in prevention and treatment of the fibrosis of the vocal fold.