SOST, an LNGFR target, inhibits the osteogenic differentiation of rat ectomesenchymal stem cells.

Objectives: The aim of this study was to investigate whether sclerostin (SOST) regulates the osteogenic differentiation of rat ectomesenchymal stem cells (EMSCs) and whether SOST and low-affinity nerve growth factor receptor (LNGFR) regulate the osteogenic differentiation of EMSCs.

Materials And Methods: EMSCs were isolated from embryonic facial processes from an embryonic 12.5-day (E12.5d) pregnant Sprague-Dawley rat. LNGFR EMSCs and LNGFR EMSCs were obtained by fluorescence-activated cell sorting and were subsequently induced to undergo osteogenic differentiation in vitro. SOST/LNGFR small-interfering RNAs and SOST/LNGFR overexpression plasmids were used to transfect EMSCs.

Results: LNGFR EMSCs displayed a higher osteogenic capacity and lower SOST levels compared with LNGFR EMSCs. SOST silencing enhanced the osteogenic differentiation of LNGFR EMSCs, while SOST overexpression attenuated the osteogenic differentiation of LNGFR EMSCs. Moreover, LNGFR was present upstream of SOST and strengthened the osteogenic differentiation of EMSCs by decreasing SOST.

Conclusions: SOST alleviated the osteogenic differentiation of EMSCs, and LNGFR enhanced the osteogenic differentiation of EMSCs by decreasing SOST, suggesting that the LNGFR/SOST pathway may be a novel target for promoting dental tissue regeneration and engineering.