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

ObjectivesThe 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 methodsEMSCs 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. ResultsLNGFR(+) 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. ConclusionsSOST 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.