PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
February 9, 20260 citations

Recombinant Humanized Collagen Type III Accelerated Palate Wound Healing by Regulating the Fibroblast Behavior via Focal Adhesion Signaling Pathway.

View Full Paper
NKNing KangMBMingXuan BaiYWYì Wáng

Key Points

  • This research aims to evaluate the effect of recombinant humanized collagen type III on wound healing in oral mucosal tissue.
  • Conducted in vitro and in vivo experiments using a mouse model.
  • Injected rhCol III solutions periwound to assess healing acceleration.
  • Performed histological evaluations to measure angiogenesis, collagen deposition, and cell proliferation.
  • Conducted RNA-sequencing to analyze the mechanism of action.
  • rhCol III significantly accelerated the healing of palate wounds compared to control.
  • Enhanced angiogenesis and collagen deposition were observed in treated wounds.
  • Increased proliferation and migration of human gingival fibroblasts and oral keratinocytes were noted.
  • Activation of the focal adhesion signaling pathway was confirmed by upregulation of vinculin and phosphorylated FAK.

Abstract

Rapid wound healing of oral soft tissue may reduce the opportunity for infection and discomfort of patients. Given that recombinant humanized collagen type III (rhCol III) is considered a nonallergenic biomaterial and can help repair skin wound healing and activate tissue remodeling, the potential effect of rhCol III on palate mucosal wound healing was preliminarily evaluated in vitro and in vivo in this study. A mouse model of an oral palate wound was established, and rhCol III solutions were injected periwound, resulting in a significant acceleration in wound healing compared to the control groups. Histological evaluation showed that rhCol III promoted angiogenesis, collagen deposition, and cell proliferation. Furthermore, the results demonstrated that rhCol III could promote human gingival fibroblast (HGF) and human oral keratinocyte (HOK) proliferation, adhesion, and migration. To further explore the mechanism, RNA-sequencing analysis results showed that rhCol III could regulate the focal adhesion signaling pathway of HGFs. The expression of vinculin and phosphorylation of FAK (Tyr397 and Tyr576) in HGFs was upregulated with rhCol III treatment. In addition, inhibition of FAK phosphorylation could inhibit HGF migration. These results suggested that rhCol III promoted HGF migration by upregulating the focal adhesion signaling pathway. These findings suggest that the topical application of rhCol III is a promising treatment for oral soft tissue wounds with the potential for future clinical use.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Kang et al. (2026) studied this question.

synapsesocial.com/papers/698979e9f0ec2af6756e7f89https://doi.org/10.1021/acsami.5c20953
Ask AI
Helpful
Bookmark
Share
View Full Paper