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Bio-Techne corporation monoclonal mouse igg 2b
Monoclonal Mouse Igg 2b, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 93/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+bmp-6+antibody/Human+BMP-6+Antibody/pmc10690547-113-2-6
Average 93 stars, based on 16 article reviews

monoclonal mouse igg 2b - by Bioz Stars, 2026-09

93/100 stars

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Article Title: Live-Cell Invasive Phenotyping Uncovers ALK2 as a Therapeutic Target in LKB1 -Mutant Lung Cancer
Article Snippet: as from Novus Biologicals. Actin (A2066) was from Sigma-Aldrich. Horseradish peroxidase–conjugated secondary Abs (Jackson ImmunoResearch) were used for Western blotting. Neutralizing BMP6 Abs (MAB507 for human, MAB6325 for mouse) were purchased from R&D Systems. LDN214117 (S7627) for in vitro and in vivo assays was from Selleckchem, and Cell Counting Kit-8 (CK04-11) was from Dojindo Laboratories.

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Relative HAMP expression in Hep3B and HepG2 cells in response to BMP6 (25 ng/ml, 6h) (A) or BMP6 + recombinant FGL1 (10µg/ml) (B). Relative ID1 expression in hepatoma cell lines treated with BMP6 and FGL1 (C). HAMP (D) and ID1 (E) expression in Hep3B cells and mouse primary hepatocytes treated for 6h with BMP6 and either Fc, full length FGL1 and the N-terminal or globular domain of FGL1. Hepatic Hamp RNA expression (F), serum hepcidin concentration (G) and liver Id1 (H) and Smad7 (I) mRNA expression in mice treated for 6 hours with saline, Fc or recombinant FGL1 (10 mg/kg) (n=5). Data shown are means ± s.e.m of three independent experiments (A- E) or treated mice and were compared for each condition to untreated cells or control mice by Student t-test. **** P < 0.0001, *** P < 0.001, ** P < 0.01, * P < 0.05.

Journal: bioRxiv

Article Title: The hepatokine FGL1 regulates hepcidin and iron metabolism during the recovery from hemorrhage-induced anemia in mice

doi: 10.1101/2023.04.06.535920

Figure Lengend Snippet: Relative HAMP expression in Hep3B and HepG2 cells in response to BMP6 (25 ng/ml, 6h) (A) or BMP6 + recombinant FGL1 (10µg/ml) (B). Relative ID1 expression in hepatoma cell lines treated with BMP6 and FGL1 (C). HAMP (D) and ID1 (E) expression in Hep3B cells and mouse primary hepatocytes treated for 6h with BMP6 and either Fc, full length FGL1 and the N-terminal or globular domain of FGL1. Hepatic Hamp RNA expression (F), serum hepcidin concentration (G) and liver Id1 (H) and Smad7 (I) mRNA expression in mice treated for 6 hours with saline, Fc or recombinant FGL1 (10 mg/kg) (n=5). Data shown are means ± s.e.m of three independent experiments (A- E) or treated mice and were compared for each condition to untreated cells or control mice by Student t-test. **** P < 0.0001, *** P < 0.001, ** P < 0.01, * P < 0.05.

Article Snippet: Proteins were eluted using Laemmli buffer and analyzed by western blot using Goat anti-Human IgG Fc fragment Secondary Antibody [HRP] (Novus biological NBP1-75006) or anti-BMP6 antibody (R&D systems, AF6325).

Techniques: Expressing, Recombinant, RNA Expression, Concentration Assay, Saline, Control

Relative expression of Hamp (A), Id1 (B), Smad7 (C) mRNA expression in mouse primary hepatocytes treated with BMP ligand (10ng/ml) and human Fc IgG2 (10µg/ml) or Fc-FGL1 (10µg/ml) for 6 hours. Data shown are means ± s.e.m of three independent experiments and were compared for each BMP between Fc or FGL1 treated cells and control cells by Two-way ANOVA. **** P < 0.0001, *** P < 0.001, ** P < 0.01, * P < 0.05. (D) Western blotting of Hep3B cells treated for 6 hours with BMP6 (10 ng/ml), ERFE (1µg/ml), or FGL1 (10µg/ml) for P-SMAD5, SMAD5 and GAPDH. (E) Western blotting of pull down assay of BMP6 and FGL1 (FL, glob, Nter) for human Fc IgG2 and BMP6.

Journal: bioRxiv

Article Title: The hepatokine FGL1 regulates hepcidin and iron metabolism during the recovery from hemorrhage-induced anemia in mice

doi: 10.1101/2023.04.06.535920

Figure Lengend Snippet: Relative expression of Hamp (A), Id1 (B), Smad7 (C) mRNA expression in mouse primary hepatocytes treated with BMP ligand (10ng/ml) and human Fc IgG2 (10µg/ml) or Fc-FGL1 (10µg/ml) for 6 hours. Data shown are means ± s.e.m of three independent experiments and were compared for each BMP between Fc or FGL1 treated cells and control cells by Two-way ANOVA. **** P < 0.0001, *** P < 0.001, ** P < 0.01, * P < 0.05. (D) Western blotting of Hep3B cells treated for 6 hours with BMP6 (10 ng/ml), ERFE (1µg/ml), or FGL1 (10µg/ml) for P-SMAD5, SMAD5 and GAPDH. (E) Western blotting of pull down assay of BMP6 and FGL1 (FL, glob, Nter) for human Fc IgG2 and BMP6.

Techniques: Expressing, Control, Western Blot, Pull Down Assay

BMP6 expression in minor salivary glands of primary Sjögren’s syndrome patients and correlation with xerostomia and sialadenitis. ( A ) Confocal images demonstrating expression of bone morphogenetic protein 6 (BMP6) in minor salivary glands (SGs) of three representative patients with primary Sjögren’s syndrome (pSS), with either low, middle or high expression (134.0, 261.3, and 797.5 fluorescence units, rows 2–4) and of one healthy volunteer (HV) (112.3 fluorescence units, row 1). Left column: slides labeled with isotype control antibody (mouse IgG) were used as background control (40× objective). Middle column: slides labeled with anti-BMP6 antibody (40× objective). Right row: Inset of the marked areas in the middle row (red dashed box). White large and small dashes were used to mark the ducts and acini tissues, respectively. ( B ) In minor SG, BMP6 positive pSS patients (BMP6 expression ≥142.3 fluorescence units, N = 43), BMP6 expression was negatively correlated with their unstimulated whole saliva (UWS) flow rate (Spearman’s r = −0.328, P = 0.0318). ( C ) In minor SG of BMP6 positive pSS patients, BMP6 expression has a trend of positive correlation with focus score (FS) but was not statistically significant (N = 20, only minor SG BMP6 positive patients whose FS data was reported by SICCA were selected. Pearson’s r = 0.3016, P = 0.1962). ( D ) In minor SG of BMP6 positive pSS patients, BMP6 expression has a trend of positive correlation with lymphocytic infiltration area (N = 43, Pearson’s r = 0.2236, P = 0.1494).

Journal: Scientific Reports

Article Title: Inhibition of bone morphogenetic protein 6 receptors ameliorates Sjögren’s syndrome in mice

doi: 10.1038/s41598-020-59443-z

Figure Lengend Snippet: BMP6 expression in minor salivary glands of primary Sjögren’s syndrome patients and correlation with xerostomia and sialadenitis. ( A ) Confocal images demonstrating expression of bone morphogenetic protein 6 (BMP6) in minor salivary glands (SGs) of three representative patients with primary Sjögren’s syndrome (pSS), with either low, middle or high expression (134.0, 261.3, and 797.5 fluorescence units, rows 2–4) and of one healthy volunteer (HV) (112.3 fluorescence units, row 1). Left column: slides labeled with isotype control antibody (mouse IgG) were used as background control (40× objective). Middle column: slides labeled with anti-BMP6 antibody (40× objective). Right row: Inset of the marked areas in the middle row (red dashed box). White large and small dashes were used to mark the ducts and acini tissues, respectively. ( B ) In minor SG, BMP6 positive pSS patients (BMP6 expression ≥142.3 fluorescence units, N = 43), BMP6 expression was negatively correlated with their unstimulated whole saliva (UWS) flow rate (Spearman’s r = −0.328, P = 0.0318). ( C ) In minor SG of BMP6 positive pSS patients, BMP6 expression has a trend of positive correlation with focus score (FS) but was not statistically significant (N = 20, only minor SG BMP6 positive patients whose FS data was reported by SICCA were selected. Pearson’s r = 0.3016, P = 0.1962). ( D ) In minor SG of BMP6 positive pSS patients, BMP6 expression has a trend of positive correlation with lymphocytic infiltration area (N = 43, Pearson’s r = 0.2236, P = 0.1494).

Article Snippet: For human minor SG and parotid SG samples: mouse anti-human BMP6 (Abcam) goat anti-human activin/ALK-2, goat anti-human BMPR-IA/ALK-3, rabbit anti-human BMPR-II antibodies (R&D Systems) were used; mouse, goat, goat and rabbit ChromPure IgG (Jackson ImmunoResearch) were used as control for BMP6, activin/ALK-2, BMPR-IA/ALK-3 and BMPR-II staining, respectively.

Techniques: Expressing, Fluorescence, Labeling, Control

Effect of ALK2/3 inhibitors on increased phosphorylated SMAD1/5/8 and SMAD2/3 expression induced by BMP6 and TGF-β in HSG cells. Phosphorylated SMAD1/5/8 (pSMAD1/5/8), pSMAD2/3, SMAD1/5/8, SMAD2 and β-actin (internal control) expression in HSG cells subjected to bone morphogenetic protein 6 (BMP6) or transforming growth factor-beta (TGF-β) with/without LDN treatment, as measured by Western blot (WB). To determine expression level, fold change of protein expression relative to control cell lysate (HSG cells treated with culture media and diluent for each BMP signaling inhibitor and diluent for LDN only) was used. ( A ) Effect of LDN-212854 on pSMAD1/5/8:SMAD1/5/8 ratio. Upper panel: representative WB of pSMAD1/5/8:SMAD1/5/8 ratio after HSG cells were cultured with 5 ng/mL TGF-β + 60 nM LDN-212854 (lane 1), 5 ng/mL TGF-β (lane 2), control medium (lane 3), 6 ng/mL BMP6 (lane 4), 6 ng/mL BMP6 + 10 nM LDN-212854 (lane 5), 25 ng/mL BMP6 (lane 6), or 25 ng/mL BMP6 + 60 nM LDN-212854 (lane 7). Lower panel: 25 ng/mL BMP6 significantly increased pSMAD1/5/8:SMAD1/5/8 ratio ( P < 0.0001), but 60 nM LDN-212854 significantly reversed this effect ( P < 0.0001); 5 ng/mL TGF-β did not change pSMAD1/5/8:SMAD1/5/8 ratio. ( B ) Effect of LDN-212854 on pSMAD2/3:SMAD2 ratio. Upper panel: representative WB of pSMAD2/3:SMAD2 ratio after HSG cells were cultured with different reagents as labeled (see legend A). Lower panel: 5 ng/mL TGF-β increased pSMAD2/3:SMAD2 ratio and 60 nM LDN-212854 did not change this effect; BMP6 with/without LDN-212854 did not alter pSMAD2/3:SMAD2 ratio. ( C ) Effect of LDN-193189 on pSMAD1/5/8:SMAD1/5/8 ratio. Upper panel: representative WB of pSMAD1/5/8:SMAD1/5/8 ratio after HSG cells were cultured with different reagents as labeled (see legend A). Lower panel: 25 ng/mL BMP6 significantly increased pSMAD1/5/8:SMAD1/5/8 ratio ( P < 0.0001), but 60 nM LDN-193189 significantly reversed this effect ( P = 0.0004); 5 ng/mL TGF-β did not change pSMAD1/5/8:SMAD1/5/8 ratio. ( D ) Effect of LDN-193189 on pSMAD2/3:SMAD2 ratio. Upper panel: representative WB of pSMAD2/3:SMAD2 ratio after HSG cells were cultured with different reagents as labeled (see legend A). Lower panel: 5 ng/mL TGF-β significantly increased pSMAD2/3:SMAD2 ratio ( P = 0.0113), but 60 nM LDN-193189 did not change this effect; BMP6 with/without LDN-212193 did not alter pSMAD2/3:SMAD2 ratio. Data shown are means ± SEM from N = 5 (A&C) or N = 2 experiments (B&D). One-way ANOVA followed by Tukey’s multiple comparison was used to compare the seven groups; * P ≤ 0.05, ** P ≤ 0.01 and *** P ≤ 0.0001 when compared with control group.

Journal: Scientific Reports

Article Title: Inhibition of bone morphogenetic protein 6 receptors ameliorates Sjögren’s syndrome in mice

doi: 10.1038/s41598-020-59443-z

Figure Lengend Snippet: Effect of ALK2/3 inhibitors on increased phosphorylated SMAD1/5/8 and SMAD2/3 expression induced by BMP6 and TGF-β in HSG cells. Phosphorylated SMAD1/5/8 (pSMAD1/5/8), pSMAD2/3, SMAD1/5/8, SMAD2 and β-actin (internal control) expression in HSG cells subjected to bone morphogenetic protein 6 (BMP6) or transforming growth factor-beta (TGF-β) with/without LDN treatment, as measured by Western blot (WB). To determine expression level, fold change of protein expression relative to control cell lysate (HSG cells treated with culture media and diluent for each BMP signaling inhibitor and diluent for LDN only) was used. ( A ) Effect of LDN-212854 on pSMAD1/5/8:SMAD1/5/8 ratio. Upper panel: representative WB of pSMAD1/5/8:SMAD1/5/8 ratio after HSG cells were cultured with 5 ng/mL TGF-β + 60 nM LDN-212854 (lane 1), 5 ng/mL TGF-β (lane 2), control medium (lane 3), 6 ng/mL BMP6 (lane 4), 6 ng/mL BMP6 + 10 nM LDN-212854 (lane 5), 25 ng/mL BMP6 (lane 6), or 25 ng/mL BMP6 + 60 nM LDN-212854 (lane 7). Lower panel: 25 ng/mL BMP6 significantly increased pSMAD1/5/8:SMAD1/5/8 ratio ( P < 0.0001), but 60 nM LDN-212854 significantly reversed this effect ( P < 0.0001); 5 ng/mL TGF-β did not change pSMAD1/5/8:SMAD1/5/8 ratio. ( B ) Effect of LDN-212854 on pSMAD2/3:SMAD2 ratio. Upper panel: representative WB of pSMAD2/3:SMAD2 ratio after HSG cells were cultured with different reagents as labeled (see legend A). Lower panel: 5 ng/mL TGF-β increased pSMAD2/3:SMAD2 ratio and 60 nM LDN-212854 did not change this effect; BMP6 with/without LDN-212854 did not alter pSMAD2/3:SMAD2 ratio. ( C ) Effect of LDN-193189 on pSMAD1/5/8:SMAD1/5/8 ratio. Upper panel: representative WB of pSMAD1/5/8:SMAD1/5/8 ratio after HSG cells were cultured with different reagents as labeled (see legend A). Lower panel: 25 ng/mL BMP6 significantly increased pSMAD1/5/8:SMAD1/5/8 ratio ( P < 0.0001), but 60 nM LDN-193189 significantly reversed this effect ( P = 0.0004); 5 ng/mL TGF-β did not change pSMAD1/5/8:SMAD1/5/8 ratio. ( D ) Effect of LDN-193189 on pSMAD2/3:SMAD2 ratio. Upper panel: representative WB of pSMAD2/3:SMAD2 ratio after HSG cells were cultured with different reagents as labeled (see legend A). Lower panel: 5 ng/mL TGF-β significantly increased pSMAD2/3:SMAD2 ratio ( P = 0.0113), but 60 nM LDN-193189 did not change this effect; BMP6 with/without LDN-212193 did not alter pSMAD2/3:SMAD2 ratio. Data shown are means ± SEM from N = 5 (A&C) or N = 2 experiments (B&D). One-way ANOVA followed by Tukey’s multiple comparison was used to compare the seven groups; * P ≤ 0.05, ** P ≤ 0.01 and *** P ≤ 0.0001 when compared with control group.

Techniques: Expressing, Control, Western Blot, Cell Culture, Labeling, Comparison

Effect of ALK2/3 inhibitors on regulatory volume decrease in HSG cells. HSG cells were placed in hypotonic solution in absence (black column) or presence of 6 ng/mL bone morphogenetic protein 6 (BMP6) (gray column), 6 ng/mL BMP6 + 0.1, 1.0 or 10 nM LDN-212854 (red columns), or 6 ng/mL BMP6 + 0.1, 1.0 or 10 nM LDN-193189 (blue columns). BMP6 significantly inhibited recovery of cell volume change (as indicated by reduced regulatory volume decrease [RVD%]), but LDN treatment reversed this effect in a dose-dependent manner. Data shown are means ± SEM from N = 3 experiments. One-way ANOVA followed by Tukey’s multiple comparison was used for comparison; * P ≤ 0.05, ** P ≤ 0.01 and *** P ≤ 0.0001 when compared with control BMP6-treated group (column 2).

Journal: Scientific Reports

Article Title: Inhibition of bone morphogenetic protein 6 receptors ameliorates Sjögren’s syndrome in mice

doi: 10.1038/s41598-020-59443-z

Figure Lengend Snippet: Effect of ALK2/3 inhibitors on regulatory volume decrease in HSG cells. HSG cells were placed in hypotonic solution in absence (black column) or presence of 6 ng/mL bone morphogenetic protein 6 (BMP6) (gray column), 6 ng/mL BMP6 + 0.1, 1.0 or 10 nM LDN-212854 (red columns), or 6 ng/mL BMP6 + 0.1, 1.0 or 10 nM LDN-193189 (blue columns). BMP6 significantly inhibited recovery of cell volume change (as indicated by reduced regulatory volume decrease [RVD%]), but LDN treatment reversed this effect in a dose-dependent manner. Data shown are means ± SEM from N = 3 experiments. One-way ANOVA followed by Tukey’s multiple comparison was used for comparison; * P ≤ 0.05, ** P ≤ 0.01 and *** P ≤ 0.0001 when compared with control BMP6-treated group (column 2).

Techniques: Comparison, Control

Saliva secretion in BMP6-overexpressing C57BL/6J mice and C57BL/6.NOD- Aec1Aec2 mice after ALK2/3 inhibitor treatment. ( A ) Submandibular glands (SMGs) of female C57BL/6J mice were cannulated and AAV5 vector encoding bone morphogenetic protein 6 (BMP6) was instilled to promote local BMP6 expression. Twenty-four months post-cannulation, mice were treated with citrate saline or 2.5 mg/kg LDN-193189 administered i.p. twice daily for 3 days. LDN-193189–treated mice showed a significant increase of salivary flow rate (SFR) compared with saline-treated mice. Data shown are means ± SEM and were analyzed with unpaired Student’s t test. ( B ) Male (M) and female (F) C57BL/6.NOD- Aec1Aec2 mice with established disease were treated daily with PBS (black columns, N = 13, 7M6F), 2.5 mg/kg LDN-212854 (red columns, N = 13, 6M7F), or 2.5 mg/kg LDN-193189 (blue columns, N = 14, 8M6F) for 24 days. SFR was determined in all mice prior to LDN treatment (day 0, baseline), and on day 3, 10, 17 and 24 thereafter. SFR significantly increased in LDN-treated mice compared with PBS-treated mice (control group) from day 10 to 24. Data shown are means ± SEM. Unpaired Student’s t test was used to compare two groups. * P < 0.05 and ** P < 0.01 compared with baseline, # P < 0.05 compared with PBS-treated group at same time point.

Journal: Scientific Reports

Article Title: Inhibition of bone morphogenetic protein 6 receptors ameliorates Sjögren’s syndrome in mice

doi: 10.1038/s41598-020-59443-z

Figure Lengend Snippet: Saliva secretion in BMP6-overexpressing C57BL/6J mice and C57BL/6.NOD- Aec1Aec2 mice after ALK2/3 inhibitor treatment. ( A ) Submandibular glands (SMGs) of female C57BL/6J mice were cannulated and AAV5 vector encoding bone morphogenetic protein 6 (BMP6) was instilled to promote local BMP6 expression. Twenty-four months post-cannulation, mice were treated with citrate saline or 2.5 mg/kg LDN-193189 administered i.p. twice daily for 3 days. LDN-193189–treated mice showed a significant increase of salivary flow rate (SFR) compared with saline-treated mice. Data shown are means ± SEM and were analyzed with unpaired Student’s t test. ( B ) Male (M) and female (F) C57BL/6.NOD- Aec1Aec2 mice with established disease were treated daily with PBS (black columns, N = 13, 7M6F), 2.5 mg/kg LDN-212854 (red columns, N = 13, 6M7F), or 2.5 mg/kg LDN-193189 (blue columns, N = 14, 8M6F) for 24 days. SFR was determined in all mice prior to LDN treatment (day 0, baseline), and on day 3, 10, 17 and 24 thereafter. SFR significantly increased in LDN-treated mice compared with PBS-treated mice (control group) from day 10 to 24. Data shown are means ± SEM. Unpaired Student’s t test was used to compare two groups. * P < 0.05 and ** P < 0.01 compared with baseline, # P < 0.05 compared with PBS-treated group at same time point.

Techniques: Plasmid Preparation, Expressing, Saline, Control

TGF-β1 from MKs induce angiogenesis via HIF-1α. ( A ) Representative images of tube formation of ECs (pre-treated TGF-β inhibitor SB431542) after addition of MKs-CM (n=6 per group). The quantitative analyses of cumulative tube length are shown in the right panel. Scale bar, 100 µm. Inh, inhibitor. ( B ) Angiographic analysis of the volume and surface area of bone vessels from TGF-β1 MK∆/∆ and TGF-β1 fl/fl mice (n=6 mice per group). Representative angiographic images are shown in the left panel. Scale bar, 1 mm. ( C ) The quantification of CD31 hi Emcn hi cells in the BM of TGF-β1 MK∆/∆ and TGF-β1 fl/fl mice (n=6 mice per group). ( D ) Flow cytometric analysis of the percentage of CD31 hi Emcn hi ECs in the BM of TGF-β1 MK∆/∆ and TGF-β1 fl/fl mice (n=6 mice per group). ( E ) Representative immunostaining images of Emcn (red) and Ki67 (green) in the BM of TGF-β1 MK∆/∆ and TGF-β1 fl/fl mice (n=6 mice per group). Scale bar, 100 µm. ( F ) Western blot analysis of the expressions of p-smad2/3, HIF-1α and VEGF in ECs (pretreated with TGF-β or HIF-1α inhibitor) after addition of MKs-CM (n=6 per group). ( G ) The concentration of VEGF in the BM of MK-deleted mice and their littermates, determined by ELISA (n = 6 mice per group). ( H ) The concentration of VEGF in the BM of TGF-β1 MK∆/∆ and TGF-β1 fl/fl mice, determined by ELISA (n=6 mice per group). Data are shown as mean ± SD. *P < 0.05, **P < 0.01. For all panels in this figure, data are representative of three independent experiments.

Journal: Theranostics

Article Title: Megakaryocytes promote bone formation through coupling osteogenesis with angiogenesis by secreting TGF-β1

doi: 10.7150/thno.40559

Figure Lengend Snippet: TGF-β1 from MKs induce angiogenesis via HIF-1α. ( A ) Representative images of tube formation of ECs (pre-treated TGF-β inhibitor SB431542) after addition of MKs-CM (n=6 per group). The quantitative analyses of cumulative tube length are shown in the right panel. Scale bar, 100 µm. Inh, inhibitor. ( B ) Angiographic analysis of the volume and surface area of bone vessels from TGF-β1 MK∆/∆ and TGF-β1 fl/fl mice (n=6 mice per group). Representative angiographic images are shown in the left panel. Scale bar, 1 mm. ( C ) The quantification of CD31 hi Emcn hi cells in the BM of TGF-β1 MK∆/∆ and TGF-β1 fl/fl mice (n=6 mice per group). ( D ) Flow cytometric analysis of the percentage of CD31 hi Emcn hi ECs in the BM of TGF-β1 MK∆/∆ and TGF-β1 fl/fl mice (n=6 mice per group). ( E ) Representative immunostaining images of Emcn (red) and Ki67 (green) in the BM of TGF-β1 MK∆/∆ and TGF-β1 fl/fl mice (n=6 mice per group). Scale bar, 100 µm. ( F ) Western blot analysis of the expressions of p-smad2/3, HIF-1α and VEGF in ECs (pretreated with TGF-β or HIF-1α inhibitor) after addition of MKs-CM (n=6 per group). ( G ) The concentration of VEGF in the BM of MK-deleted mice and their littermates, determined by ELISA (n = 6 mice per group). ( H ) The concentration of VEGF in the BM of TGF-β1 MK∆/∆ and TGF-β1 fl/fl mice, determined by ELISA (n=6 mice per group). Data are shown as mean ± SD. *P < 0.05, **P < 0.01. For all panels in this figure, data are representative of three independent experiments.

Article Snippet: In some assays, neutralizing antibodies against TGF-β1 (9016; R&D, Minneapolis, Minnesota, USA ), VEGF (AF-493; R&D), BMP6 (MAB6325; R&D), IGF-1 (AF791; R&D), PDGF-BB (ab34074; Abcam), CXCl12 (79014; R&D), BMP2 (MAB111; R&D), TGF-β2 (AB-112-NA; R&D), TGF-β3 (20724; R&D), BMP4 (MAB50201; R&D) and IgG (AB-108-C; R&D) were added to the MKs-CM.

Techniques: Immunostaining, Western Blot, Concentration Assay, Enzyme-linked Immunosorbent Assay

MKs attenuate irradiation-induced bone loss in mice by secreting TGF-β1. ( A ) The concentrations of TGF-β1 and osteocalcin in the BM of sham or irradiated mice 2 months after treated with MKs or TPO, determined by ELISA (n=6 mice per group). ( B ) Quantitative Micro-CT analysis of the BMD, BV/TV and Ct.Th of femora from sham or irradiated mice 2 months after treated with MKs or TPO (n=6 mice per group). ( C ) HE staining demonstrating the layers of endosteal osteoblasts in the BM from sham or irradiated mice 2 weeks after treated with MKs or TPO (n=6 mice per group). Scale bar, 200 µm. ( D ) Quantification of osteocalcin + cell numbers on surface of TB and EB from sham or irradiated mice 2 months after treated with MKs or TPO (n=6 mice per group). ( E ) Von Kossa staining showing the mineralization of bone matrix in sham or irradiated mice 2 months after treated with MKs or TPO (n=6 mice per group). Scale bar, 50 µm. ( F ) The concentration of VEGF in the BM of sham or irradiated mice 2 months after treated with MKs or TPO, determined by ELISA (n=6 mice per group). ( G ) Angiographic analysis of the volume and surface area of bone vessels from sham or irradiated mice 2 months after treated with MKs or TPO (n=6 mice per group). ( H ) Representative Micro-CT images of longitudinal section femurs, cross-sectional view of the distal femurs and reconstructed trabecular structure of the ROI (White dashed box) in TGF-β1 MK∆/∆ mice with or without radioactive bone injury 2 months after treatment of TPO. Color scale bar represents bone mineral density level. (n=6 mice per group). Data are shown as mean ± SD. *P < 0.05, **P < 0.01. ns, no significant. For all panels in this figure, data are representative of three independent experiments.

Journal: Theranostics

Article Title: Megakaryocytes promote bone formation through coupling osteogenesis with angiogenesis by secreting TGF-β1

doi: 10.7150/thno.40559

Figure Lengend Snippet: MKs attenuate irradiation-induced bone loss in mice by secreting TGF-β1. ( A ) The concentrations of TGF-β1 and osteocalcin in the BM of sham or irradiated mice 2 months after treated with MKs or TPO, determined by ELISA (n=6 mice per group). ( B ) Quantitative Micro-CT analysis of the BMD, BV/TV and Ct.Th of femora from sham or irradiated mice 2 months after treated with MKs or TPO (n=6 mice per group). ( C ) HE staining demonstrating the layers of endosteal osteoblasts in the BM from sham or irradiated mice 2 weeks after treated with MKs or TPO (n=6 mice per group). Scale bar, 200 µm. ( D ) Quantification of osteocalcin + cell numbers on surface of TB and EB from sham or irradiated mice 2 months after treated with MKs or TPO (n=6 mice per group). ( E ) Von Kossa staining showing the mineralization of bone matrix in sham or irradiated mice 2 months after treated with MKs or TPO (n=6 mice per group). Scale bar, 50 µm. ( F ) The concentration of VEGF in the BM of sham or irradiated mice 2 months after treated with MKs or TPO, determined by ELISA (n=6 mice per group). ( G ) Angiographic analysis of the volume and surface area of bone vessels from sham or irradiated mice 2 months after treated with MKs or TPO (n=6 mice per group). ( H ) Representative Micro-CT images of longitudinal section femurs, cross-sectional view of the distal femurs and reconstructed trabecular structure of the ROI (White dashed box) in TGF-β1 MK∆/∆ mice with or without radioactive bone injury 2 months after treatment of TPO. Color scale bar represents bone mineral density level. (n=6 mice per group). Data are shown as mean ± SD. *P < 0.05, **P < 0.01. ns, no significant. For all panels in this figure, data are representative of three independent experiments.

Techniques: Irradiation, Enzyme-linked Immunosorbent Assay, Micro-CT, Staining, Concentration Assay

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