Bidirectional regulation of i-type lysozyme on cutaneous wound healing

Biomed Pharmacother. 2020 Nov:131:110700. doi: 10.1016/j.biopha.2020.110700. Epub 2020 Oct 7.

Abstract

Objective: This study aimed to assess the effect and mechanism of i-type lysozyme on cutaneous wound healing animal model and Multiple cell models both in vivo and in vitro.

Methods: Therefore, to evaluate its regenerative efficacy on wound healing process, we daily applied i-type lysozyme on murine full-thickness excisional wounds. After sacrifice on indicated days, skin tissues around surgical defects were harvested and assessed for re-epithelialization, granulation tissue formation, neovascularization and remodeling. To elucidate the underlying mechanisms, i-type lysozyme was analyzed for its tissue regenerative potency on the proliferation, invasion, migration and tube formation against keratinocytes, fibroblasts and endothelial cells. Antioxidant and antimicrobial experiments were also conducted to elucidate protective ability of i-type lysozyme to wound bed.

Results: It displayed excellent bi-directional regulation in wound repair, with significant acceleration of epidermal and dermal regeneration as well as the efficient attenuation of excessive collagen deposition and fibrosis in the surgical lesion. I-type lysozyme treatment augmented the proliferation and migration of HaCaT, NIH 3T3 and HUVECs, enhanced the invasion of HaCaT and HUVECs as well as accelerated tube formation of HUVECs. Additionally, it significantly recovered the proliferation of H2O2-damaged cells, whereas represented no microbicidal effect under effective concentration of wound healing.

Conclusion: Our findings demonstrate the bi-directional regulation of i-type lysozyme in wound healing process through promoting tissue regeneration while hampering scar formation, implying that it is a promising therapeutic agent for wound repair.

Keywords: Angiogenesis; Fibrogenesis; I-type lysozyme; Re-Epithelialization; Scar formation; Wound healing.

MeSH terms

  • Animals
  • Cell Movement / drug effects
  • Collagen / metabolism
  • HaCaT Cells
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Keratinocytes / drug effects
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Muramidase / pharmacology*
  • NIH 3T3 Cells
  • Re-Epithelialization / drug effects
  • Regeneration / drug effects
  • Wound Healing / drug effects*
  • Wound Healing / physiology

Substances

  • Collagen
  • Muramidase