Fig 1: circRFWD2/miR-6817-5p/BMPR2 axis could regulate the osteogenesis of hDPSCs through Smad5 and p38 phosphorylation. (A) Western blot analyses of phosphorylated Smad5 (p-Smad5), Smad5, phosphorylated p-38 (p-p38), p38, and the internal control GAPDH in si-NC and si-circRFWD2 groups. (B) The protein levels of p-Smad5, Smad5, p-p38, p38, and GAPDH in si-NC and si-circRFWD2 groups. (C) Western blot analyses of p-Smad5, Smad5, p-p38, p38, and GAPDH in miR-NC, miR-6817-5p mimic, and miR-6817-5p inhibitor groups. (D) The protein levels of p-Smad5, Smad5, p-p38, p38, and GAPDH in miR-NC, miR-6817-5p mimic, and miR-6817-5p inhibitor groups. (E) Western blot analyses of p-Smad5, Smad5, p-p38, p38, and GAPDH in si-NC and si-BMPR2 groups. (F) The protein levels of p-Smad5, Smad5, p-p38, p38, and GAPDH in si-NC and si-BMPR2 groups. (G) Schematic model showed that miR-6817-5p, targeted by circRFWD2, suppressed osteogenic differentiation through the BMPR2-mediated activation of pSmad5 and p38 MAPK pathway. All experiments were repeated at least three times. The data are shown as the mean ± SD (n = 3). **P < 0.01. NC: negative control; p-Smad5: phosphorylated Smad5; p-p38: phosphorylated p-38.