Recombinant human collagen XVII promotes skin repair and regeneration by upregulating Lgr6 signaling pathway.
Summary
In laser-injury and UVB photoaging models, 0.1% recombinant human collagen XVII enhanced skin repair by expanding Lgr6+ epidermal stem cells and activating Wnt/β-catenin signaling. It reduced epidermal thickening and restored skin architecture, providing a mechanistic basis for regenerative dermatology applications.
Key Findings
- 0.1% rhCOL17 was the optimal concentration for promoting repair in laser-injury and UVB photoaging models.
- rhCOL17 expanded Lgr6-positive epidermal stem cells and reduced epidermal thickening.
- Mechanistically, rhCOL17 upregulated Lgr6 and activated downstream Wnt/β-catenin signaling.
Clinical Implications
Formulating rhCOL17 (around 0.1%) could enhance epidermal repair after procedures (e.g., fractional lasers) or UV-induced damage; translation requires human safety/efficacy trials and optimized delivery.
Why It Matters
This study identifies a COL17–Lgr6–Wnt axis driving epidermal regeneration in vivo, pointing to a tractable biomaterial for photoaging and wound repair. It advances mechanistic understanding and therapeutic development in regenerative and cosmetic dermatology.
Limitations
- Preclinical models without human clinical validation
- Dose–response and long-term safety in humans are unknown
Future Directions
Conduct phase I/II trials of topical/locally delivered rhCOL17, define pharmacokinetics and skin penetration, and validate Lgr6/Wnt activation in human skin.
Study Information
- Study Type
- Basic/mechanistic research
- Research Domain
- Pathophysiology
- Evidence Level
- V - Preclinical in vivo mechanistic study using animal models
- Study Design
- OTHER