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. 2017 Sep 22;25(2):268–281. doi: 10.1038/cdd.2017.153

Figure 9.

Figure 9

VnP-16 substantially alleviates osteoporosis by reversing OVX-induced bone loss. (a–d) μCT reconstruction of metaphyses of distal femurs (a) as well as BMD (b), BV/TV (c), and trabecular number (d) in OVX mice at 1 week after administration of vehicle, rhBMP-2, SP, or VnP-16. The images represent femurs (a, upper panel) and its trabecular bones (a, lower panel) of vehicle-, rhBMP-2-, or peptide-treated OVX mice. (e and f) Masson’s trichrome (e) and H&E (f) staining of femur sections from OVX mice at 1 week after administration of vehicle, rhBMP-2, SP, or VnP-16. Scale bars, 200 μm. (g and h) Morphometric analysis of the osteoblast number (g) and osteoblast surface (h) in OVX mice at 1 week after administration of vehicle, rhBMP-2, SP, or VnP-16. (i) TRAP staining of osteoclasts surrounding trabecular bones in OVX mice at 1 week after administration of vehicle, rhBMP-2, SP, or VnP-16. Scale bars, 200 μm. (j and k) Morphometric analysis of the osteoclast number (j) and osteoclast surface (k) in OVX mice at 1 week after administration of vehicle, rhBMP-2, SP, or VnP-16. (l) Proposed pathway for reversing estrogen deficiency-induced bone loss by a vitronectin-derived peptide VnP-16. OB, osteoblasts; OC, osteoclasts; M, bone marrow-derived macrophages. Data in (b–d, g, h, j and k) represent the mean±SD (n=7 per group). *P<0.05, **P<0.01