Kangfuxin accelerates extraction socket healing by promoting angiogenesis via upregulation of CCL2 in stem cells.
Zheng-Rong GaoYing-Hui ZhouYa-Qiong ZhaoJie ZhaoQin YeShao-Hui ZhangYao FengLi TanQiong LiuYun ChenZe-Yue OuyangJing HuMarie Aimee DusengeYun-Zhi FengYue GuoPublished in: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research (2023)
Kangfuxin (KFX) shows potential in wound healing but its role in socket healing is unclear. This research finds increased bone mass, mineralization, and collagen deposition in KFX-treated mice. Mouse bone marrow mesenchymal stem cells, human periodontal ligament stem cells (hPDLSCs), and human dental pulp stem cells (hDPSCs) are treated with KFX under osteogenic induction. RNA-sequencing reveals upregulated chemokine-related genes, with a three-fold increase in chemokine (C-C motif) ligand 2 (Ccl2). The conditioned medium (CM) of hPDLSCs and hDPSCs treated with KFX promotes endothelial cell migration and angiogenesis. Ccl2 knockdown abolishes CM-induced endothelial cell migration and angiogenesis, which can be reversed by recombinant CCL2 treatment. KFX-treated mice showed increased vasculature. In conclusion, KFX increases the expression of CCL2 in stem cells, promoting bone formation and mineralization in the extraction socket by inducing endothelial cell angiogenesis. This article is protected by copyright. All rights reserved.
Keyphrases
- endothelial cells
- stem cells
- cell migration
- high glucose
- liver fibrosis
- wound healing
- liver injury
- vascular endothelial growth factor
- drug induced
- poor prognosis
- cell therapy
- high fat diet induced
- mesenchymal stem cells
- cell proliferation
- newly diagnosed
- climate change
- induced pluripotent stem cells
- oxidative stress
- type diabetes
- long non coding rna
- smoking cessation
- binding protein
- cell free