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. 2016 Jan 1;12(1):63–71. doi: 10.7150/ijbs.12690

Figure 1.

Figure 1

The uPA deficiency promotes inflammatory osteoclastogenesis and bone destruction. 25 mg/kg LPS was administered subcutaneously into the shaved back of the male mice. The administration was carried out weekly for up to 4 weeks. (A) The BMD in the femurs of the LPS-administered male uPA+/+ and uPA-/- mice was obtained from pQCT measurement (saline or LPS-administered uPA+/+ mice, n=9; saline or LPS-administered uPA-/- mice, n=8). (B) The TRAP-staining of femurs in the LPS-administered male uPA+/+ and uPA-/- mice. (C) The intensity of TRAP-staining on the decalcified sections in the LPS-administered male uPA+/+ and uPA-/- mice was quantitatively evaluated as described in the Materials and Methods (n=6). (D) Bone marrow-derived cells from the uPA+/+ and uPA-/- mice were cultured for 3 days in the presence of LPS (1 μg/ml) and M-CSF (100 ng/ml). Then, TRAP-staining was performed to detect mature OCs. (E) Mature OCs were identified as multinucleated TRAP-positive cells (n=4). (F) Bone marrow-derived cells from the uPA-/- mice were cultured for 3 days with LPS (1 μg/ml), M-CSF (100 ng/ml), and with or without uPA (10 nM). Then, TRAP-staining was performed to detect mature OCs. (G) Mature OCs in the uPA-/- mice were identified as multinucleated TRAP-positive cells (n=3). The data represent the mean ± SEM. *, P<0.01; **, P<0.05; NS, not significant. Scale bar = 200 μm.