Nano-dicalcium silicate promotes angiogenesis via enhancing endothelial cell proliferation, migration and tube...

Bone defects, especially critical-sized ones, pose a significant challenge in clinical orthopedics due to their impaired self-regeneration ability. Our previous experiments have confirmed that dicalcium silicate nanoparticles(nC₂S) exhibit excellent osteogenic activity, but whether they also possesses good angiogenic activity remains unelucidated. In this study, we established a co-culture model of nC2S and HUVECs to further explore its angiogenic effect. CCK-8 assay, immunofluorescence (IF) staining, and Western Blotting (WB) analysis were utilized to systematically assess the effects of nC₂S on the proliferative capacity, migratory potential, and tube formation ability of HUVECs-three core functional hallmarks of angiogenesis. In vivo, nC₂S scaffolds were implanted into bone defect models to validate their ability in promoting neovascularization within bone defect sites. Furthermore, RNA sequencing was employed to explore the potential molecular mechanisms of nC₂S-induced angiogenesis. We found that nC2S can promote HUVECs proliferation, migration, and tube formation. RNA-seq result showed upregulation of MAPK, PI3K/Akt pathway. Thus, we speculate that nC₂S may promote angiogenesis through cell proliferation. This study aims to investigate the role of dicalcium silicate in promoting angiogenesis during bone defect repair, and to provide an important theoretical basis and practical guidance for the development of novel bone regeneration materials.