Transgenic high expression of EphB4 in canine periodontal ligament stem cells modulates osteogenic differentiation and migration in cPDLSCs

转基因高表达犬牙周膜干细胞中的EphB4可调节cPDLSCs的成骨分化和迁移

阅读:4

Abstract

BACKGROUND: Signaling molecules play a critical role in regulating stem cell-mediated bone regeneration. In this study, we investigated the effect of EphB4 gene transfection on the osteogenic differentiation and migratory capacity of canine periodontal ligament stem cells (cPDLSCs). Using a lentiviral vector, we established stable EphB4-overexpressing cPDLSCs and evaluated their functional properties in vitro and regenerative potential in vivo. RESULTS: Our results demonstrated that EphB4 transfection significantly enhanced the osteogenic capability of cPDLSCs, as evidenced by elevated expression of osteogenic markers-osteocalcin, Runx2, and collagen type I-along with increased mineral deposition. Furthermore, EphB4 overexpression strongly promoted cell migration, indicating roles in enhancing cell homing and recruitment. Mechanistic analyses indicated that these effects were associated with greater EphB4 phosphorylation, suggesting activation of forward signaling pathways. In a canine alveolar bone defect model, transplantation of EphB4-modified cPDLSCs led to significantly augmented bone regeneration compared with control groups. Micro-computed tomography analysis revealed greater bone volume/total volume ratio, increased trabecular number and thickness, and reduced trabecular separation. Histological and immunohistochemical analyses confirmed greater expression of osteogenic proteins in the EphB4 group; no significant differences were observed between the two control groups (untreated cPDLSCs and empty vector-transduced cPDLSCs). CONCLUSIONS: These findings collectively indicate that EphB4 overexpression potentiates the osteogenic and migratory properties of cPDLSCs, thereby promoting alveolar bone repair in vivo. Our results highlight the therapeutic potential of EphB4 for periodontal and bone regeneration applications.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。