Researchers at Pitt are investigating the use of a ‘stop scarring’ signaling molecule decorin, a small leucine-rich proteoglycan, as a therapeutic to reduce scarring. The extracellular matrix (ECM) and its associated components are important in cutaneous wound healing. Compelling data in in a mouse model of hypertrophic scarring supports the important role of decorin as a regulator of collagen fibrillogenesis and a non-competitive inhibitor of multiple growth factors signaling cascades.
Description
The researchers utilized a slow-release coacervate system to administer decorin in the mouse model. The findings indicated that the decorin group had the same early wound closure as the control, AND led to much more complete wound resolution, as indicated by significantly reduced cutaneous thickness, enhanced collagen alignment, and improved overall wound scoring in the mice. These results suggested that decorin could be a promising alternative therapy for patients likely to scar after wounds.
Applications
- Improved wound healing
Advantages
The use of controlled delivery methods is significant for therapeutic approaches for improving wound healing outcomes and minimizing scarring. The research outlines the potential of decorin as a promising tool for improving wound healing outcomes and minimizing hypertrophic scarring in clinical settings.
Invention Readiness
This technology is at the level of preclinical animal model data. The study involved using a mouse model of hypertrophic scarring, focusing on the role of decorin in regulating the wound healing process. The experimental design included intradermal injections of decorin embedded in a slow-release coacervate system. The researchers compared the outcomes of decorin treatment with coacervate-only baseline and HB-EGF treated control mice. The results demonstrated that decorin treatment led to better healing outcomes and could potentially limit the hypertrophic scarring phenotype observed in the control groups.
IP Status
https://patents.google.com/patent/WO2023183816A2
