Transcription factor 7-like 2 promotes osteogenic differentiation and boron-induced bone repair via lipocalin 2.

Boron-containing mesoporous bioactive glass (B-MBG) scaffolds could be capable of promoting osteogenesis by activating Wnt/β-catenin signaling pathway during the process of bone defect repair. Despite this, more involving molecular controls are still largely unclear. In the present study, we identified that the downstream of Wnt/β-catenin signaling pathway named transcription factor 7-like 2 (TCF7L2) served as a key effector to promote boron-induced bone regeneration and osteogenesis through lipocalin 2 (LCN2). TCF7L2 was highly expressed in osteoblasts when treated with B-MBG scaffold extraction than MBG. LCN2, as a secreted bone factor, positively affected osteogenic differentiation of MC3T3-E1 and osteogenesis in vivo , which could be induced by TCF7L2. In addition, interference of TCF7L2 decreased the osteogenic differentiation of osteoblasts. Finally, we identified that rLCN2 could rescue the poor ability of osteogenic differentiation of MC3T3-E1 whose Tcf7l2 gene was knocked down by lentiviral transfection of shRNA. Our findings provide some new insights into the molecular controls of boron-associated bone regeneration and potential therapeutic targets for the treatment of bone defects. Unlabelled Image • TCF7L2, the downstream of β-catenin in Wnt/β-catenin pathway, could promote boron-induced osteogenesis for B-MBG scaffolds. • TCF7L2 had positive effects on osteogenesis during the process of normal bone development. • The positive role of TCF7L2 for boron-induced and normal osteogenesis related to the increasing of LCN2 in osteoblasts. • LCN2 played a positive role in osteogenic differentiation in osteoblasts as the downstream of TCF7L2. • Recombinant LCN2 could rescue the poor ability of osteogenic differentiation in MC3T3-E1 lacking tcf7l2 gene. [ABSTRACT FROM AUTHOR]