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.

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