伤口愈合
焦点粘着
成纤维细胞
角质形成细胞
磷酸化
长春新碱
细胞生物学
皮肤修复
癌症研究
粘附
信号转导
细胞粘附
重组DNA
化学
医学
细胞迁移
口腔粘膜
真皮成纤维细胞
人体皮肤
生物材料
免疫学
Ⅰ型胶原
病理
作者
Ning Kang,MingXuan Bai,Jing Wang,Lü Chen,Yan Xu,Ping Gong,Kangqi Zhang,Hai Lin,Xingdong Zhang
标识
DOI:10.1021/acsami.5c20953
摘要
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.
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