Extended Data Fig. 3: Influence of RANKL-binding molecules on the osteogenic effects of mOC-SEVs.
From: Coupling of bone resorption and formation by RANKL reverse signalling
a, The inhibitory effect of OPG on the activation of PI3K–Akt–mTORC1 pathway in ST2 cells stimulated with mOC-SEVs. Akt Thr308 phosphorylation (p-Akt), PRAS40 Thr246 phosphorylation (p-PRAS40) and S6K1 Thr389 phosphorylation (p-S6K1) indicate PI3K, Akt and mTORC1 activation, respectively. b, The inhibitory effect of OPG on osteoblast-marker expression levels in ST2 cells after 5 days of stimulation with mOC-SEVs (n = 3). c, Von Kossa-stained ST2 cells stimulated with mOC-SEVs or vehicle in the presence or absence of OPG. d, Inhibitory effect of the WP9QY peptide, αR-tri, or OPG on RANK-Fc binding to GST–sRANKL immobilized on ELISA plate (n = 3 biologically independent samples). e, Von Kossa-stained primary osteoblasts derived from RANKL-deficient mice or wild-type littermates stimulated with mOC-SEVs, WP9QY peptide, mOC-SEVs plus WP9QY peptide, or vehicle. f, mRNA expression levels of osteoblast markers in primary osteoblasts derived from RANKL-deficient mice or wild-type littermates after 5 days of stimulation with mOC-SEVs, WP9QY peptide, mOC-SEVs plus WP9QY peptide, or vehicle (n = 3). In b, f, data are mean, with individual points representing biologically independent samples. One-way ANOVA followed by Student–Newman–Keuls test; *P < 0.05, **P < 0.01.
