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1.
Figure 4

Figure 4. From: Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.

Rgs12 is essential for OC differentiation. (a) TRAP staining of control and CD11b;Rgs12fl/fl OCs derived from bone marrow OC precursor cells in response to RANKL and M-CSF. (b) Quantification of the number of TRAP+ multinucleated OCs (MNCs) shown in panel (a) (n=4, P<0.001). (c) OC differentiation from control and CD11b;Rgs12fl/fl bone marrow cells in coculture with wild-type OBs. (d) Quantification of the number of TRAP+ MNCs shown in (c) (n=4, P<0.001)

X Yuan, et al. Cell Death Differ. 2015 Dec;22(12):2046-2057.
2.
Figure 1

Figure 1. From: Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.

Deletion of Rgs12 in hematopoietic cells (Mx1;Rgs12fl/fl) and OCs (CD11b;Rgs12fl/fl) reduces Rgs12 expression. (a and d) PCR of spleen genomic DNA showed the deletion allele of Rgs12 in Mx1;Rgs12fl/fl and CD11b;Rgs12fl/fl mice. (b and e) qPCR results showed less Rgs12 mRNA expression in the spleen of Mx1;Rgs12fl/fl and CD11b-positive bone marrow cells of CD11b;Rgs12fl/fl. The expression of Rgs12 was normalized to GAPDH (glyceraldehyde 3-phosphate dehydrogenase) expression (n=3, ***P<0.001 versus controls). (c and f) Western blotting analysis of Rgs12 expression in the bone marrow cells of Mx1;Rgs12fl/fl and CD11b-positive bone marrow cells of CD11b;Rgs12fl/fl

X Yuan, et al. Cell Death Differ. 2015 Dec;22(12):2046-2057.
3.
Figure 8

Figure 8. From: Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.

Mx1;Rgs12fl/fl were partially protected from OVX-induced bone loss. (a) Tibias from sham-operated and OVX mice were examined by μCT. (b) Quantitative analysis of bone volume/tissue volume (BV/TV, %), trabecular thickness (Tb.Th, μm), trabecular number (Tb.N, /mm), and trabecular separation (Tb.Sp, μm) in the tibia of Mx1;Rgs12fl/fl and Mx1;Rgs12+/+ mice in the OVX and sham groups shown in panel (a) (n=5). (c) Quantification of BFR/BS (mm3/mm2/day) and the MAR (μd/day). Data represent mean±S.D. n=5. *P<0.05; ***P<0.001 compared with Mx1;Rgs12+/+ sham. #P<0.01 Mx1;Rgs12fl/fl OVX versus Mx1;Rgs12fl/fl sham; P<0.01 Mx1;Rgs12fl/fl OVX versus Mx1;Rgs12+/+ OVX

X Yuan, et al. Cell Death Differ. 2015 Dec;22(12):2046-2057.
4.
Figure 5

Figure 5. From: Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.

Rgs12 is essential for OC function. (a) F-actin ring staining of OCs generated from the bone marrow cells of control and CD11b;Rgs12fl/fl mice. (b) Quantification of the number of OCs with intact actin rings or impaired rings illustrated in panel (a) (n=3, P<0.01). (c) F-actin ring staining of OCs from control and CD11b;Rgs12fl/fl bone marrow cells in coculture with wild-type OBs. (d) Quantification of the number of OCs with actin rings illustrated in panel (c) (n=3, P<0.01). (e) Bone resorption lacunae on dentin slices formed by control and Rgs12Null OCs. (f) Quantification of the resorption area shown in panel (e) (n=3, P<0.001). **P<0.01, ***P<0.001

X Yuan, et al. Cell Death Differ. 2015 Dec;22(12):2046-2057.
5.
Figure 3

Figure 3. From: Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.

Deletion of Rgs12 in OCs (CD11b;Rgs12fl/fl) causes a significant increase in bone mass. (a) μCT analysis of the femurs of 3-month-old CD11b;Rgs12fl/fl and CD11b;Rgs12fl/+. (b) Quantitative analysis of BV/TV (%), Tb.Th (μm), Tb.N (/mm), and Tb.Sp (μm) in the tibia of CD11b;Rgs12fl/fl and CD11b;Rgs12fl/+ mice shown in panel (a). Results are mean±S.D. (n=4, **P<0.01, ***P<0.001). (c) Hematoxylin and eosin staining of the proximal tibia metaphyseal regions of CD11b;Rgs12fl/fl and CD11b;Rgs12fl/+ mice at 3 months. (d) Quantitative analysis of the percentage of bone area to total bone marrow space shown in panel (c) (n=4, P<0.001). (e) TRAP staining of tibiae sections shown in panel (c) to identify OCs. (f) Histomorphometric analysis of OCs in CD11b;Rgs12fl/fl and CD11b;Rgs12fl/+ mice at 3 months of age. n=4, **P<0.01, ***P<0.001

X Yuan, et al. Cell Death Differ. 2015 Dec;22(12):2046-2057.
6.
Figure 7

Figure 7. From: Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.

Loss of Rgs12 in OC precursor cells reduced LPS-induced bone loss in vivo and OC formation in vitro. (a) Hematoxylin and eosin staining of calvarial bone injected with PBS (sham) or LPS in CD11b;Rgs12fl/+ and CD11b;Rgs12fl/fl mice. (b) Quantification of the percentage of eroded surface over total bone surface shown in panel (a) (n=8). (c) TRAP staining of the calvarial bone shown in panel (a) to assess OC numbers. (d) Quantification of the number of OC per bone surface shown in panel (c) (n=8). **P<0.01, ***P<0.001 compared with CD11b;Rgs12fl/++sham; #P<0.001 CD11b;Rgs12fl/fl+LPS versus CD11b;Rgs12fl/fl; P<0.001: CD11b;Rgs12fl/fl+LPS versus CD11b;Rgs12fl/++LPS. (e) TRAP staining of the OC generated by M-CSF/RANKL or M-CSF/LPS as indicated. (f) Quantification of the TRAP+ MNCs shown in panel (e) (n=3). ***P<0.001, *P<0.05 compared with CD11b;Rgs12fl/++RNAKL; P<0.001: CD11b;Rgs12fl/fl+LPS versus CD11b;Rgs12fl/++LPS

X Yuan, et al. Cell Death Differ. 2015 Dec;22(12):2046-2057.
7.
Figure 2

Figure 2. From: Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.

Deletion of Rgs12 in hematopoietic cells (Mx1;Rgs12fl/fl) causes a significant increase in bone mass with reduced OC formation. (a) μCT analysis of the femurs of 3-month-old Mx1;Rgs12fl/fl and Mx1;Rgs12+/+ (upper photograph: longitudinal view; lower photograph: axial view of the metaphyseal region). An apparent increase in the bone mass was observed in Mx1;Rgs12fl/fl mice compared with Mx1;Rgs12+/+ mice. (b) Quantitative analysis of bone volume/tissue volume (BV/TV, %), trabecular thickness (Tb.Th, μm), trabecular number (Tb.N, /mm) and trabecular separation (Tb.Sp, μm) in the tibia of Mx1;Rgs12fl/fl and Mx1;Rgs12+/+ mice shown in panel (a). Results are mean±S.D. (n=4, ***P<0.001). (c) Hematoxylin and eosin staining of the proximal tibia metaphyseal regions of 3-month-old Mx1;Rgs12fl/fl and Mx1;Rgs12+/+ mice. (d) Quantitative analysis of the percentage of bone area to total bone marrow space shown in panel (c) (n=4, P<0.001). (e) TRAP staining of tibiae sections shown in panel (c) to identify OCs. (f) Histomorphometric analysis of osteoclasts in Mx1;Rgs12fl/fl and Mx1;Rgs12+/+ mice at 3 months of age (n=4, P<0.001). N.Oc/B.Pm: number of OCs/bone perimeter (mm); Oc.S/B.S: OC surface/bone surface (%)

X Yuan, et al. Cell Death Differ. 2015 Dec;22(12):2046-2057.
8.
Figure 6

Figure 6. From: Regulators of G protein signaling 12 promotes osteoclastogenesis in bone remodeling and pathological bone loss.

Deletion of Rgs12 inhibits NFAT2, c-Fos, and Cathepsin K expression and blocks Ca2+ oscillations; and ectopic expression of NFAT2 rescues defective OC differentiation. (a) qPCR analysis of OC marker gene NFAT2, c-Fos, and Cathepsin K (CatK) expression. GAPDH (glyceraldehyde 3-phosphate dehydrogenase) was used as a loading control, and the expression level of control was set as 1 (n=3). (b) Analysis of Ca2+ oscillations in OCs generated from control and CD11b;Rgs12fl/fl mice at 24 h after RANKL stimulation. Five cells from each group were traced, calculated, and plotted with the time indicated by different colors. (c) qPCR analysis of NFAT2 expression in OCs from CD11b;Rgs12fl/+ and CD11b;Rgs12fl/fl treated with (Ca-NFAT2) or without (Ctrl) Ca-NFAT2 retrovirus. GAPDH was used as a loading control, and the expression level of control was set as 1 (n=3). (d) TRAP staining of CD11b;Rgs12fl/+ and CD11b;Rgs12fl/fl OCs formed by bone marrow OC precursor cells with or without ca-NFAT2 retrovirus as indicated. (e) Quantification of the number of TRAP+ MNCs shown in panel (d) (n=3). (f) qPCR analysis of c-Fos and CatK expression in OC derived from CD11b;Rgs12fl/+ and CD11b;Rgs12fl/fl bone marrow OC precursor cells treated with or without Ca-NFAT2 retrovirus. GAPDH was used as a loading control, and the expression level of CD11b;Rgs12fl/+ was set as 1 (n=3). ***P<0.001, *P<0.05 compared with CD11b;Rgs12+/fl; #P<0.01 CD11b;Rgs12fl/fl+NFAT2 versus CD11b;Rgs12fl/fl; P<0.01 CD11b;Rgs12fl/fl+NFAT2 versus CD11b;Rgs12fl/++NFAT2

X Yuan, et al. Cell Death Differ. 2015 Dec;22(12):2046-2057.

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