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    Structured Review

    R&D Systems pdgf bb
    Continuous intraosseous administration of SCS prevents glucocorticoid-induced bone degeneration. ( A ) Schematic illustration of the glucocorticoid (GC; MPS)-induced bone deterioration and intraosseous SCS treatment. ( B-D ) Representative H&E staining images of the femur at 6 weeks (B). Magnified views of the cortical bone and trabecular bone in the marrow cavity are shown on the right. Solid arrows indicate normal osteocytes, while hollow arrows indicate empty osteocyte lacunae. Quantification of empty lacunae ratios in cortical bone (C) and trabecular bone (D). n = 6 biological replicates. (Scale bars, 500 μm and 25 μm) ( E-H ) Representative immunofluorescence staining of OPN + mature osteoblasts, osteolectin + osteoprogenitors, and VE-cadherin + endothelial cells (ECs) in femur at 6 weeks (E), and corresponding quantifications (F–H). n = 6 biological replicates. (Scale bars, 100 μm and 20 μm) ( I and J ) Representative flow cytometry plots of capillary subtypes in the femur (I), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (J). n = 6 biological replicates. ( K and L ) Flow cytometry plots showing Sca-1 hi CD31 hi arteriolar ECs (K), and corresponding quantification (L). n = 6 biological replicates. ( M and N ) Representative micro-CT 3D images of the femur (M). Quantitative analysis of percent bone volume (BV/TV) (N). n = 6 biological replicates. (Scale bars, 1.5 mm, 600 μm and 545 μm) ( O and P ) ELISA analysis of VEGF (O) <t>and</t> <t>PDGF-BB</t> (P) levels in bone marrow supernatant and peripheral serum from PBS- and SCS-treated groups at week 6. n = 6 biological replicates. ( Q ) ELISA quantification of the osteogenic factor osteocalcin in peripheral serum at week 6. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, F, G, H, J, L, N, O, P and Q ).
    Pdgf Bb, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 61 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pdgf+bb/Mouse%2FRat+PDGF-BB+Quantikine+ELISA+Kit/pmc12859453-603-9-10
    Average 94 stars, based on 61 article reviews
    pdgf bb - by Bioz Stars, 2026-10
    94/100 stars

    Images

    1) Product Images from "Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming"

    Article Title: Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2025.11.039

    Continuous intraosseous administration of SCS prevents glucocorticoid-induced bone degeneration. ( A ) Schematic illustration of the glucocorticoid (GC; MPS)-induced bone deterioration and intraosseous SCS treatment. ( B-D ) Representative H&E staining images of the femur at 6 weeks (B). Magnified views of the cortical bone and trabecular bone in the marrow cavity are shown on the right. Solid arrows indicate normal osteocytes, while hollow arrows indicate empty osteocyte lacunae. Quantification of empty lacunae ratios in cortical bone (C) and trabecular bone (D). n = 6 biological replicates. (Scale bars, 500 μm and 25 μm) ( E-H ) Representative immunofluorescence staining of OPN + mature osteoblasts, osteolectin + osteoprogenitors, and VE-cadherin + endothelial cells (ECs) in femur at 6 weeks (E), and corresponding quantifications (F–H). n = 6 biological replicates. (Scale bars, 100 μm and 20 μm) ( I and J ) Representative flow cytometry plots of capillary subtypes in the femur (I), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (J). n = 6 biological replicates. ( K and L ) Flow cytometry plots showing Sca-1 hi CD31 hi arteriolar ECs (K), and corresponding quantification (L). n = 6 biological replicates. ( M and N ) Representative micro-CT 3D images of the femur (M). Quantitative analysis of percent bone volume (BV/TV) (N). n = 6 biological replicates. (Scale bars, 1.5 mm, 600 μm and 545 μm) ( O and P ) ELISA analysis of VEGF (O) and PDGF-BB (P) levels in bone marrow supernatant and peripheral serum from PBS- and SCS-treated groups at week 6. n = 6 biological replicates. ( Q ) ELISA quantification of the osteogenic factor osteocalcin in peripheral serum at week 6. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, F, G, H, J, L, N, O, P and Q ).
    Figure Legend Snippet: Continuous intraosseous administration of SCS prevents glucocorticoid-induced bone degeneration. ( A ) Schematic illustration of the glucocorticoid (GC; MPS)-induced bone deterioration and intraosseous SCS treatment. ( B-D ) Representative H&E staining images of the femur at 6 weeks (B). Magnified views of the cortical bone and trabecular bone in the marrow cavity are shown on the right. Solid arrows indicate normal osteocytes, while hollow arrows indicate empty osteocyte lacunae. Quantification of empty lacunae ratios in cortical bone (C) and trabecular bone (D). n = 6 biological replicates. (Scale bars, 500 μm and 25 μm) ( E-H ) Representative immunofluorescence staining of OPN + mature osteoblasts, osteolectin + osteoprogenitors, and VE-cadherin + endothelial cells (ECs) in femur at 6 weeks (E), and corresponding quantifications (F–H). n = 6 biological replicates. (Scale bars, 100 μm and 20 μm) ( I and J ) Representative flow cytometry plots of capillary subtypes in the femur (I), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (J). n = 6 biological replicates. ( K and L ) Flow cytometry plots showing Sca-1 hi CD31 hi arteriolar ECs (K), and corresponding quantification (L). n = 6 biological replicates. ( M and N ) Representative micro-CT 3D images of the femur (M). Quantitative analysis of percent bone volume (BV/TV) (N). n = 6 biological replicates. (Scale bars, 1.5 mm, 600 μm and 545 μm) ( O and P ) ELISA analysis of VEGF (O) and PDGF-BB (P) levels in bone marrow supernatant and peripheral serum from PBS- and SCS-treated groups at week 6. n = 6 biological replicates. ( Q ) ELISA quantification of the osteogenic factor osteocalcin in peripheral serum at week 6. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, F, G, H, J, L, N, O, P and Q ).

    Techniques Used: Staining, Immunofluorescence, Flow Cytometry, Micro-CT, Enzyme-linked Immunosorbent Assay

    SCS targets downstream senescent lineage commitment of bone marrow MSCs to mitigate GC-induced bone deterioration. ( A ) Schematic diagram illustrating the experimental design: CD45 − Ter119 − CD31 − LepR + MSCs isolated from mice co-treated with SCS and MPS for 7 days were subjected to in vitro lineage-competitive differentiation, followed by DEX-induced senescence in lineage-mixed cells. These cells were then adoptively transplanted into healthy bone marrow cavity to assess bone deterioration development. ( B ) Representative H&E-stained images of the femur 12 weeks after adoptive transfer. PBS-DEX group: LepR + MSCs from PBS and MPS co-treated mice subjected to in vitro lineage differentiation and DEX-induced senescence, followed by transplantation. SCS-DEX group: LepR + MSCs from SCS and MPS co-treated mice processed similarly. PBS group: solvent control without cell transplantation. Solid arrows indicate intact osteocytes; hollow arrows indicate empty lacunae. (Scale bars, 250 μm and 25 μm) ( C – E ) Quantitative analysis of marrow hypertrophic adipocyte diameter (C), proportion of empty osteocyte lacunae in trabecular bone (D), and adipocyte number (E) in the metaphysis 12 weeks post-transplantation. n = 19 biological replicates (C), n = 6 biological replicates (D), n = 8 biological replicates (E). ( F ) Quantification of empty lacunae in epiphysis at 12 weeks post-transplantation. n = 6 biological replicates. ( G – I ) Representative flow cytometry plots of capillary ECs subtypes in the femur at 12 weeks (G), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (H) and CD45 − Ter119 − CD31 lo Emcn lo ECs (I). n = 6 biological replicates. ( J and K ) Representative flow cytometry plots (J) and corresponding quantification (K) of CD45 − Ter119 − Sca-1 hi CD31 hi arteriolar ECs in the femur at 12 weeks post-transplantation. n = 6 biological replicates. ( L ) Representative micro-CT images of the femur at 12 weeks post-transplantation across different treatment groups. (Scale bars, 1.5 mm and 500 μm) ( M – P ) Quantitative analysis of bone parameters in the metaphysis: bone mineral density (BMD) (M), percent bone volume (BV/TV) (N), trabecular separation (Tb.Sp) (O), and trabecular number (Tb.N) (P). n = 6 biological replicates. ( Q ) Serum ELISA analysis of the osteogenic marker osteocalcin at 12 weeks post-transplantation. n = 6 biological replicates. ( R and S ) ELISA analysis of PDGF-BB (R) and VEGF (S) in both bone marrow supernatant and peripheral serum at 12 weeks post-transplantation. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, E, F, H, I, K, M, N, O, P, Q, R and S ).
    Figure Legend Snippet: SCS targets downstream senescent lineage commitment of bone marrow MSCs to mitigate GC-induced bone deterioration. ( A ) Schematic diagram illustrating the experimental design: CD45 − Ter119 − CD31 − LepR + MSCs isolated from mice co-treated with SCS and MPS for 7 days were subjected to in vitro lineage-competitive differentiation, followed by DEX-induced senescence in lineage-mixed cells. These cells were then adoptively transplanted into healthy bone marrow cavity to assess bone deterioration development. ( B ) Representative H&E-stained images of the femur 12 weeks after adoptive transfer. PBS-DEX group: LepR + MSCs from PBS and MPS co-treated mice subjected to in vitro lineage differentiation and DEX-induced senescence, followed by transplantation. SCS-DEX group: LepR + MSCs from SCS and MPS co-treated mice processed similarly. PBS group: solvent control without cell transplantation. Solid arrows indicate intact osteocytes; hollow arrows indicate empty lacunae. (Scale bars, 250 μm and 25 μm) ( C – E ) Quantitative analysis of marrow hypertrophic adipocyte diameter (C), proportion of empty osteocyte lacunae in trabecular bone (D), and adipocyte number (E) in the metaphysis 12 weeks post-transplantation. n = 19 biological replicates (C), n = 6 biological replicates (D), n = 8 biological replicates (E). ( F ) Quantification of empty lacunae in epiphysis at 12 weeks post-transplantation. n = 6 biological replicates. ( G – I ) Representative flow cytometry plots of capillary ECs subtypes in the femur at 12 weeks (G), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (H) and CD45 − Ter119 − CD31 lo Emcn lo ECs (I). n = 6 biological replicates. ( J and K ) Representative flow cytometry plots (J) and corresponding quantification (K) of CD45 − Ter119 − Sca-1 hi CD31 hi arteriolar ECs in the femur at 12 weeks post-transplantation. n = 6 biological replicates. ( L ) Representative micro-CT images of the femur at 12 weeks post-transplantation across different treatment groups. (Scale bars, 1.5 mm and 500 μm) ( M – P ) Quantitative analysis of bone parameters in the metaphysis: bone mineral density (BMD) (M), percent bone volume (BV/TV) (N), trabecular separation (Tb.Sp) (O), and trabecular number (Tb.N) (P). n = 6 biological replicates. ( Q ) Serum ELISA analysis of the osteogenic marker osteocalcin at 12 weeks post-transplantation. n = 6 biological replicates. ( R and S ) ELISA analysis of PDGF-BB (R) and VEGF (S) in both bone marrow supernatant and peripheral serum at 12 weeks post-transplantation. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, E, F, H, I, K, M, N, O, P, Q, R and S ).

    Techniques Used: Isolation, In Vitro, Staining, Adoptive Transfer Assay, Transplantation Assay, Solvent, Control, Flow Cytometry, Micro-CT, Enzyme-linked Immunosorbent Assay, Marker

    Related Articles

    Incubation:

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    Article Snippet: To assess integrin activation, vSMCs were pretreated with mouse or human Seroblock (BD Biosciences, San Jose, CA, USA) for 15 min at RT in HBSS buffer containing 0.1% BSA, 0.5 mM CaCl 2 and MgCl 2 . .. Next, vSMCs were incubated with mAbs to activation‐dependent epitopes on the β 1 integrin subunit: mouse vSMCs: rat anti‐CD29 (clone 9EG7) [ ] followed by goat anti‐rat IgG‐PE; human vSMCs: anti‐CD29‐PE (clone HUTS‐21) (BD Biosciences, San Jose, CA, USA) [ , ] and with mAbs to total β 1 ‐integrin subunit mouse vSMCs: anti‐CD29‐FITC (clone MB1.2) (Millipore‐Sigma, Cuyahoga Heights, OH, USA); human vSMCs: anti‐CD29‐PE (clone MAR4) (BD Biosciences, San Jose, CA, USA) in the absence or presence of PDGF‐BB (50 ng/mL) (R&D Systems, Minneapolis, MN, USA) for 30 min at 37°C. αVβ3 activation was assessed by soluble Fg‐AF647 binding (30 μg/mL) (ThermoFisher Scientific, Waltham, MA, USA) and its total expression with anti‐human CD51/61‐AF488 (clone LM609) (EM Millipore, Burlington, MA, USA) on HASMCs and anti‐mouse CD61‐FITC (clone 2C9/G2) (BD Pharmingen, Franklin Lakes, NJ, USA) on mouse vSMCs. .. Fg and antibody binding were measured with BD FACSSymphony A5 SE flow cytometer and analyzed using a FlowJo software v10.9 (BD Biosciences, San Jose, CA, USA).

    Article Title: Hyperglycemia-Reduced Platelet-Derived Growth Factor–BB Expression Impairs Corneal Wound Healing in Diabetic Mice
    Article Snippet: .. Cells were seeded into 96-well plates at 5,000 cells/well and incubated for 24 hours under the following conditions: PDGF-BB (40 ng/mL; PeproTech), anti–PDGF-BB neutralizing antibody (8 μg/mL; R&D Systems), PDGF-BB–specific small interfering RNA (siRNA) (siPDGF-BB, 25 nM; Dharmacon, Lafayette, CO, USA), or nontargeting control siRNA (siNC, 25 nM). .. Cell viability was measured using a CCK-8 assay kit (Abbkine, Wuhan, China).

    Article Title: Kindlin‐2 Deletion in Mural Cells Leads to Vascular Instability
    Article Snippet: To assess integrin activation, vSMCs were pretreated with mouse or human Seroblock (BD Biosciences, San Jose, CA, USA) for 15 min at RT in HBSS buffer containing 0.1% BSA, 0.5 mM CaCl2 and MgCl2. .. Next, vSMCs were incubated with mAbs to activation- dependent epitopes on the β1 integrin subunit: mouse vSMCs: rat anti- CD29 (clone 9EG7) [39] followed by goat antirat IgG- PE; human vSMCs: anti- CD29- PE (clone HUTS- 21) (BD Biosciences, San Jose, CA, USA) [40, 41] and with mAbs to total β1- integrin subunit mouse vSMCs: anti- CD29- FITC (clone MB1.2) (Millipore- Sigma, Cuyahoga Heights, OH, USA); human vSMCs: anti- CD29- PE (clone MAR4) (BD Biosciences, San Jose, CA, USA) in the absence or presence of PDGF- BB (50 ng/mL) (R&D Systems, Minneapolis, MN, USA) for 30 min at 37°C. αVβ3 activation was assessed by soluble Fg- AF647 binding (30 μg/mL) (ThermoFisher Scientific, Waltham, MA, USA) and its total expression with anti- human CD51/61- AF488 (clone LM609) (EM Millipore, Burlington, MA, USA) on HASMCs and anti- mouse CD61- FITC (clone 2C9/G2) (BD Pharmingen, Franklin Lakes, NJ, USA) on mouse vSMCs. .. Fg and antibody binding were measured with BD FACSSymphony A5 SE flow cytometer and analyzed using a FlowJo software v10.9 (BD Biosciences, San Jose, CA, USA).

    Activation Assay:

    Article Title: Kindlin‐2 Deletion in Mural Cells Leads to Vascular Instability
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    Article Title: Kindlin‐2 Deletion in Mural Cells Leads to Vascular Instability
    Article Snippet: To assess integrin activation, vSMCs were pretreated with mouse or human Seroblock (BD Biosciences, San Jose, CA, USA) for 15 min at RT in HBSS buffer containing 0.1% BSA, 0.5 mM CaCl2 and MgCl2. .. Next, vSMCs were incubated with mAbs to activation- dependent epitopes on the β1 integrin subunit: mouse vSMCs: rat anti- CD29 (clone 9EG7) [39] followed by goat antirat IgG- PE; human vSMCs: anti- CD29- PE (clone HUTS- 21) (BD Biosciences, San Jose, CA, USA) [40, 41] and with mAbs to total β1- integrin subunit mouse vSMCs: anti- CD29- FITC (clone MB1.2) (Millipore- Sigma, Cuyahoga Heights, OH, USA); human vSMCs: anti- CD29- PE (clone MAR4) (BD Biosciences, San Jose, CA, USA) in the absence or presence of PDGF- BB (50 ng/mL) (R&D Systems, Minneapolis, MN, USA) for 30 min at 37°C. αVβ3 activation was assessed by soluble Fg- AF647 binding (30 μg/mL) (ThermoFisher Scientific, Waltham, MA, USA) and its total expression with anti- human CD51/61- AF488 (clone LM609) (EM Millipore, Burlington, MA, USA) on HASMCs and anti- mouse CD61- FITC (clone 2C9/G2) (BD Pharmingen, Franklin Lakes, NJ, USA) on mouse vSMCs. .. Fg and antibody binding were measured with BD FACSSymphony A5 SE flow cytometer and analyzed using a FlowJo software v10.9 (BD Biosciences, San Jose, CA, USA).

    Binding Assay:

    Article Title: Kindlin‐2 Deletion in Mural Cells Leads to Vascular Instability
    Article Snippet: To assess integrin activation, vSMCs were pretreated with mouse or human Seroblock (BD Biosciences, San Jose, CA, USA) for 15 min at RT in HBSS buffer containing 0.1% BSA, 0.5 mM CaCl 2 and MgCl 2 . .. Next, vSMCs were incubated with mAbs to activation‐dependent epitopes on the β 1 integrin subunit: mouse vSMCs: rat anti‐CD29 (clone 9EG7) [ ] followed by goat anti‐rat IgG‐PE; human vSMCs: anti‐CD29‐PE (clone HUTS‐21) (BD Biosciences, San Jose, CA, USA) [ , ] and with mAbs to total β 1 ‐integrin subunit mouse vSMCs: anti‐CD29‐FITC (clone MB1.2) (Millipore‐Sigma, Cuyahoga Heights, OH, USA); human vSMCs: anti‐CD29‐PE (clone MAR4) (BD Biosciences, San Jose, CA, USA) in the absence or presence of PDGF‐BB (50 ng/mL) (R&D Systems, Minneapolis, MN, USA) for 30 min at 37°C. αVβ3 activation was assessed by soluble Fg‐AF647 binding (30 μg/mL) (ThermoFisher Scientific, Waltham, MA, USA) and its total expression with anti‐human CD51/61‐AF488 (clone LM609) (EM Millipore, Burlington, MA, USA) on HASMCs and anti‐mouse CD61‐FITC (clone 2C9/G2) (BD Pharmingen, Franklin Lakes, NJ, USA) on mouse vSMCs. .. Fg and antibody binding were measured with BD FACSSymphony A5 SE flow cytometer and analyzed using a FlowJo software v10.9 (BD Biosciences, San Jose, CA, USA).

    Article Title: Kindlin‐2 Deletion in Mural Cells Leads to Vascular Instability
    Article Snippet: To assess integrin activation, vSMCs were pretreated with mouse or human Seroblock (BD Biosciences, San Jose, CA, USA) for 15 min at RT in HBSS buffer containing 0.1% BSA, 0.5 mM CaCl2 and MgCl2. .. Next, vSMCs were incubated with mAbs to activation- dependent epitopes on the β1 integrin subunit: mouse vSMCs: rat anti- CD29 (clone 9EG7) [39] followed by goat antirat IgG- PE; human vSMCs: anti- CD29- PE (clone HUTS- 21) (BD Biosciences, San Jose, CA, USA) [40, 41] and with mAbs to total β1- integrin subunit mouse vSMCs: anti- CD29- FITC (clone MB1.2) (Millipore- Sigma, Cuyahoga Heights, OH, USA); human vSMCs: anti- CD29- PE (clone MAR4) (BD Biosciences, San Jose, CA, USA) in the absence or presence of PDGF- BB (50 ng/mL) (R&D Systems, Minneapolis, MN, USA) for 30 min at 37°C. αVβ3 activation was assessed by soluble Fg- AF647 binding (30 μg/mL) (ThermoFisher Scientific, Waltham, MA, USA) and its total expression with anti- human CD51/61- AF488 (clone LM609) (EM Millipore, Burlington, MA, USA) on HASMCs and anti- mouse CD61- FITC (clone 2C9/G2) (BD Pharmingen, Franklin Lakes, NJ, USA) on mouse vSMCs. .. Fg and antibody binding were measured with BD FACSSymphony A5 SE flow cytometer and analyzed using a FlowJo software v10.9 (BD Biosciences, San Jose, CA, USA).

    Expressing:

    Article Title: Kindlin‐2 Deletion in Mural Cells Leads to Vascular Instability
    Article Snippet: To assess integrin activation, vSMCs were pretreated with mouse or human Seroblock (BD Biosciences, San Jose, CA, USA) for 15 min at RT in HBSS buffer containing 0.1% BSA, 0.5 mM CaCl 2 and MgCl 2 . .. Next, vSMCs were incubated with mAbs to activation‐dependent epitopes on the β 1 integrin subunit: mouse vSMCs: rat anti‐CD29 (clone 9EG7) [ ] followed by goat anti‐rat IgG‐PE; human vSMCs: anti‐CD29‐PE (clone HUTS‐21) (BD Biosciences, San Jose, CA, USA) [ , ] and with mAbs to total β 1 ‐integrin subunit mouse vSMCs: anti‐CD29‐FITC (clone MB1.2) (Millipore‐Sigma, Cuyahoga Heights, OH, USA); human vSMCs: anti‐CD29‐PE (clone MAR4) (BD Biosciences, San Jose, CA, USA) in the absence or presence of PDGF‐BB (50 ng/mL) (R&D Systems, Minneapolis, MN, USA) for 30 min at 37°C. αVβ3 activation was assessed by soluble Fg‐AF647 binding (30 μg/mL) (ThermoFisher Scientific, Waltham, MA, USA) and its total expression with anti‐human CD51/61‐AF488 (clone LM609) (EM Millipore, Burlington, MA, USA) on HASMCs and anti‐mouse CD61‐FITC (clone 2C9/G2) (BD Pharmingen, Franklin Lakes, NJ, USA) on mouse vSMCs. .. Fg and antibody binding were measured with BD FACSSymphony A5 SE flow cytometer and analyzed using a FlowJo software v10.9 (BD Biosciences, San Jose, CA, USA).

    Article Title: Kindlin‐2 Deletion in Mural Cells Leads to Vascular Instability
    Article Snippet: To assess integrin activation, vSMCs were pretreated with mouse or human Seroblock (BD Biosciences, San Jose, CA, USA) for 15 min at RT in HBSS buffer containing 0.1% BSA, 0.5 mM CaCl2 and MgCl2. .. Next, vSMCs were incubated with mAbs to activation- dependent epitopes on the β1 integrin subunit: mouse vSMCs: rat anti- CD29 (clone 9EG7) [39] followed by goat antirat IgG- PE; human vSMCs: anti- CD29- PE (clone HUTS- 21) (BD Biosciences, San Jose, CA, USA) [40, 41] and with mAbs to total β1- integrin subunit mouse vSMCs: anti- CD29- FITC (clone MB1.2) (Millipore- Sigma, Cuyahoga Heights, OH, USA); human vSMCs: anti- CD29- PE (clone MAR4) (BD Biosciences, San Jose, CA, USA) in the absence or presence of PDGF- BB (50 ng/mL) (R&D Systems, Minneapolis, MN, USA) for 30 min at 37°C. αVβ3 activation was assessed by soluble Fg- AF647 binding (30 μg/mL) (ThermoFisher Scientific, Waltham, MA, USA) and its total expression with anti- human CD51/61- AF488 (clone LM609) (EM Millipore, Burlington, MA, USA) on HASMCs and anti- mouse CD61- FITC (clone 2C9/G2) (BD Pharmingen, Franklin Lakes, NJ, USA) on mouse vSMCs. .. Fg and antibody binding were measured with BD FACSSymphony A5 SE flow cytometer and analyzed using a FlowJo software v10.9 (BD Biosciences, San Jose, CA, USA).

    Small Interfering RNA:

    Article Title: Hyperglycemia-Reduced Platelet-Derived Growth Factor–BB Expression Impairs Corneal Wound Healing in Diabetic Mice
    Article Snippet: .. Cells were seeded into 96-well plates at 5,000 cells/well and incubated for 24 hours under the following conditions: PDGF-BB (40 ng/mL; PeproTech), anti–PDGF-BB neutralizing antibody (8 μg/mL; R&D Systems), PDGF-BB–specific small interfering RNA (siRNA) (siPDGF-BB, 25 nM; Dharmacon, Lafayette, CO, USA), or nontargeting control siRNA (siNC, 25 nM). .. Cell viability was measured using a CCK-8 assay kit (Abbkine, Wuhan, China).

    Control:

    Article Title: Hyperglycemia-Reduced Platelet-Derived Growth Factor–BB Expression Impairs Corneal Wound Healing in Diabetic Mice
    Article Snippet: .. Cells were seeded into 96-well plates at 5,000 cells/well and incubated for 24 hours under the following conditions: PDGF-BB (40 ng/mL; PeproTech), anti–PDGF-BB neutralizing antibody (8 μg/mL; R&D Systems), PDGF-BB–specific small interfering RNA (siRNA) (siPDGF-BB, 25 nM; Dharmacon, Lafayette, CO, USA), or nontargeting control siRNA (siNC, 25 nM). .. Cell viability was measured using a CCK-8 assay kit (Abbkine, Wuhan, China).

    Article Title: Ginsenoside compound K exerts osteoprotective effects by suppressing osteoclastogenesis and promoting preosteoclast PDGF-BB-induced angiogenesis via targeting CSF1R.
    Article Snippet: We previously found that oral administration of Panax notoginseng saponins (PNS) alleviated bone loss in ovariectomy(OVX)-induced osteoporotic mice.. However, the specific active component responsible for this effect and its underlying mechanism remained unclear.. Ginsenoside compound K (CK), one of the main active components of PNS, may serve as a promising therapeutic agent for osteoporosis.

    Article Title: In Vitro Enhanced Performance of Human Platelet Lysate Gel Integrated with Mesoporous Silica Nanoparticle/Carboxymethyl Chitosan Composite Hydrogel: Structural Stability and Biological Activities for Chronic Wound Healing
    Article Snippet: .. To unequivocally determine the role of PDGF-BB specifically as a primary GF mediating hPL-induced periodontal fibroblast migration, PDGF-BB activity was inhibited by preincubating xPMC/hPLG spots with 0.2 μg/mL of a PDGF-BB neutralizing antibody (AF-220-NA, R&D Systems) for 45 min. As a negative control, xPMC/hPLG spots were pretreated for 45 min with an isotype control goat IgG antibody (0.2 μg/mL; AB-108 C, R&D Systems). .. To unequivocally determine the role of PDGF-BB specifically as a primary GF mediating hPL-induced periodontal fibroblast migration, PDGF-BB activity was inhibited by preincubating xPMC/hPLG spots with 0.2 μg/mL of a PDGF-BB neutralizing antibody (AF-220-NA, R&D Systems) for 45 min. As a negative control, xPMC/hPLG spots were pretreated for 45 min with an isotype control goat IgG antibody (0.2 μg/mL; AB-108 C, R&D Systems).

    Recombinant:

    Article Title: Durotaxis is a driver and potential therapeutic target in lung fibrosis and metastatic pancreatic cancer
    Article Snippet: F-actin and nuclei were stained with Alexa Fluor 546– phalloidin and 4′,6-diamidino-2-phenylindole (DAPI) (Invitrogen), respectively. .. Antibody dilutions were prepared according to the manufacturer's guidelines Mouse and human recombinant TGF-β1 and PDGF-BB were purchased from R&D Systems, and 18:1 LPA was purchased from Avanti Polar Lipids. .. Fibronectin and collagen type I were obtained from Sigma-Aldrich.

    Enzyme-linked Immunosorbent Assay:

    Article Title: Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming
    Article Snippet: .. Levels of angiogenesis-associated factors, including VEGF (Neobioscience, EMC103.96) and PDGF-BB (R&D Systems, MBB00), were quantified in both bone marrow supernatants and serum using ELISA kits according to the manufacturer's instructions. .. Serum concentrations of the osteogenic marker osteocalcin (NOVUS, NBP2-68151) were also measured.

    Migration:

    Article Title: In Vitro Enhanced Performance of Human Platelet Lysate Gel Integrated with Mesoporous Silica Nanoparticle/Carboxymethyl Chitosan Composite Hydrogel: Structural Stability and Biological Activities for Chronic Wound Healing
    Article Snippet: .. To unequivocally determine the role of PDGF-BB specifically as a primary GF mediating hPL-induced periodontal fibroblast migration, PDGF-BB activity was inhibited by preincubating xPMC/hPLG spots with 0.2 μg/mL of a PDGF-BB neutralizing antibody (AF-220-NA, R&D Systems) for 45 min. As a negative control, xPMC/hPLG spots were pretreated for 45 min with an isotype control goat IgG antibody (0.2 μg/mL; AB-108 C, R&D Systems). .. To unequivocally determine the role of PDGF-BB specifically as a primary GF mediating hPL-induced periodontal fibroblast migration, PDGF-BB activity was inhibited by preincubating xPMC/hPLG spots with 0.2 μg/mL of a PDGF-BB neutralizing antibody (AF-220-NA, R&D Systems) for 45 min. As a negative control, xPMC/hPLG spots were pretreated for 45 min with an isotype control goat IgG antibody (0.2 μg/mL; AB-108 C, R&D Systems).

    Activity Assay:

    Article Title: In Vitro Enhanced Performance of Human Platelet Lysate Gel Integrated with Mesoporous Silica Nanoparticle/Carboxymethyl Chitosan Composite Hydrogel: Structural Stability and Biological Activities for Chronic Wound Healing
    Article Snippet: .. To unequivocally determine the role of PDGF-BB specifically as a primary GF mediating hPL-induced periodontal fibroblast migration, PDGF-BB activity was inhibited by preincubating xPMC/hPLG spots with 0.2 μg/mL of a PDGF-BB neutralizing antibody (AF-220-NA, R&D Systems) for 45 min. As a negative control, xPMC/hPLG spots were pretreated for 45 min with an isotype control goat IgG antibody (0.2 μg/mL; AB-108 C, R&D Systems). .. To unequivocally determine the role of PDGF-BB specifically as a primary GF mediating hPL-induced periodontal fibroblast migration, PDGF-BB activity was inhibited by preincubating xPMC/hPLG spots with 0.2 μg/mL of a PDGF-BB neutralizing antibody (AF-220-NA, R&D Systems) for 45 min. As a negative control, xPMC/hPLG spots were pretreated for 45 min with an isotype control goat IgG antibody (0.2 μg/mL; AB-108 C, R&D Systems).

    Negative Control:

    Article Title: In Vitro Enhanced Performance of Human Platelet Lysate Gel Integrated with Mesoporous Silica Nanoparticle/Carboxymethyl Chitosan Composite Hydrogel: Structural Stability and Biological Activities for Chronic Wound Healing
    Article Snippet: .. To unequivocally determine the role of PDGF-BB specifically as a primary GF mediating hPL-induced periodontal fibroblast migration, PDGF-BB activity was inhibited by preincubating xPMC/hPLG spots with 0.2 μg/mL of a PDGF-BB neutralizing antibody (AF-220-NA, R&D Systems) for 45 min. As a negative control, xPMC/hPLG spots were pretreated for 45 min with an isotype control goat IgG antibody (0.2 μg/mL; AB-108 C, R&D Systems). .. To unequivocally determine the role of PDGF-BB specifically as a primary GF mediating hPL-induced periodontal fibroblast migration, PDGF-BB activity was inhibited by preincubating xPMC/hPLG spots with 0.2 μg/mL of a PDGF-BB neutralizing antibody (AF-220-NA, R&D Systems) for 45 min. As a negative control, xPMC/hPLG spots were pretreated for 45 min with an isotype control goat IgG antibody (0.2 μg/mL; AB-108 C, R&D Systems).



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    Image Search Results


    SLC7A5 is upregulated during vascular remodeling. (A) Volcano plot of the GSE220512 dataset showing that Slc7a5 is significantly upregulated in neointimal tissue from mouse carotid arteries at Day 7 after wire injury compared with Day 0 controls. (B) Quantitative PCR analysis of SLC7A5 mRNA expression at indicated time points. (C) Representative Western blot and quantitative analysis showing SLC7A5 protein expression at 0, 7, and 14 days after vascular injury (n = 6). (D) Immunohistochemical staining of SLC7A5 in vascular tissues from sham, 7-day, and 14-day groups, showing increased expression in the medial layer during remodeling. bar = 50 μm. (E) Western blot and quantification of SLC7A5 expression in endothelial cells (ECs), macrophages, and vascular smooth muscle cells (VSMCs) (n = 3). (F) Immunofluorescence staining showing increased SLC7A5 expression in VSMCs following PDGF-BB stimulation compared with control. bar = 50 μm. Data are presented as mean ± SEM. Statistical significance is indicated as shown.

    Journal: Frontiers in Pharmacology

    Article Title: SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway

    doi: 10.3389/fphar.2026.1857850

    Figure Lengend Snippet: SLC7A5 is upregulated during vascular remodeling. (A) Volcano plot of the GSE220512 dataset showing that Slc7a5 is significantly upregulated in neointimal tissue from mouse carotid arteries at Day 7 after wire injury compared with Day 0 controls. (B) Quantitative PCR analysis of SLC7A5 mRNA expression at indicated time points. (C) Representative Western blot and quantitative analysis showing SLC7A5 protein expression at 0, 7, and 14 days after vascular injury (n = 6). (D) Immunohistochemical staining of SLC7A5 in vascular tissues from sham, 7-day, and 14-day groups, showing increased expression in the medial layer during remodeling. bar = 50 μm. (E) Western blot and quantification of SLC7A5 expression in endothelial cells (ECs), macrophages, and vascular smooth muscle cells (VSMCs) (n = 3). (F) Immunofluorescence staining showing increased SLC7A5 expression in VSMCs following PDGF-BB stimulation compared with control. bar = 50 μm. Data are presented as mean ± SEM. Statistical significance is indicated as shown.

    Article Snippet: JPH203 (KYT-0353) provided by Targetmol was dissolved in DMSO to prepare stock solution,and PDGF-BB from MCE (HY-P7278) was reconstituted in sterile normal saline according to the manufacturer’s instructions.

    Techniques: Real-time Polymerase Chain Reaction, Expressing, Western Blot, Immunohistochemical staining, Staining, Immunofluorescence, Control

    Knockdown of SLC7A5 inhibits PDGF-BB–induced VSMC proliferation, migration, and phenotypic switching. (A) Western blot analysis and quantification of PCNA expression in VSMCs under different treatments (n = 4). (B) Representative images of EdU staining and quantification of EdU-positive cells (n = 4) bar = 50 μm. (C) Western blot analysis and quantification of MMP2 expression (n = 4). (D) Representative images of wound healing assays at indicated time points and quantitative analysis of migration rate (n = 4) bar = 50 μm. (E) Western blot analysis and quantification of α-SMA expression (n = 4). (F) Representative immunofluorescence staining of α-SMA (green) and DAPI (blue), along with quantitative analysis of fluorescence intensity (n = 4) bar = 100 μm. PDGF-BB was used to induce VSMC activation. siSLC7A5 was used to silence SLC7A5 expression, and siNC served as a negative control. Data were presented as mean ± SEM from at four independent experiments. Statistical significance was determined using one-way ANOVA followed by appropriate post hoc tests.

    Journal: Frontiers in Pharmacology

    Article Title: SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway

    doi: 10.3389/fphar.2026.1857850

    Figure Lengend Snippet: Knockdown of SLC7A5 inhibits PDGF-BB–induced VSMC proliferation, migration, and phenotypic switching. (A) Western blot analysis and quantification of PCNA expression in VSMCs under different treatments (n = 4). (B) Representative images of EdU staining and quantification of EdU-positive cells (n = 4) bar = 50 μm. (C) Western blot analysis and quantification of MMP2 expression (n = 4). (D) Representative images of wound healing assays at indicated time points and quantitative analysis of migration rate (n = 4) bar = 50 μm. (E) Western blot analysis and quantification of α-SMA expression (n = 4). (F) Representative immunofluorescence staining of α-SMA (green) and DAPI (blue), along with quantitative analysis of fluorescence intensity (n = 4) bar = 100 μm. PDGF-BB was used to induce VSMC activation. siSLC7A5 was used to silence SLC7A5 expression, and siNC served as a negative control. Data were presented as mean ± SEM from at four independent experiments. Statistical significance was determined using one-way ANOVA followed by appropriate post hoc tests.

    Article Snippet: JPH203 (KYT-0353) provided by Targetmol was dissolved in DMSO to prepare stock solution,and PDGF-BB from MCE (HY-P7278) was reconstituted in sterile normal saline according to the manufacturer’s instructions.

    Techniques: Knockdown, Migration, Western Blot, Expressing, Staining, Immunofluorescence, Fluorescence, Activation Assay, Negative Control

    SLC7A5 knockdown attenuates the activation of the PI3K/Akt signaling pathway induced by PDGF-BB. (A–C) Western blot analysis of PI3K/Akt signaling pathway–related proteins, including phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), and total Akt.

    Journal: Frontiers in Pharmacology

    Article Title: SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway

    doi: 10.3389/fphar.2026.1857850

    Figure Lengend Snippet: SLC7A5 knockdown attenuates the activation of the PI3K/Akt signaling pathway induced by PDGF-BB. (A–C) Western blot analysis of PI3K/Akt signaling pathway–related proteins, including phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), and total Akt.

    Article Snippet: JPH203 (KYT-0353) provided by Targetmol was dissolved in DMSO to prepare stock solution,and PDGF-BB from MCE (HY-P7278) was reconstituted in sterile normal saline according to the manufacturer’s instructions.

    Techniques: Knockdown, Activation Assay, Western Blot

    Inhibition of SLC7A5 suppresses PDGF-BB–induced VSMC activation and PI3K/Akt signaling in vitro . (A) Western blot analysis and quantification of PCNA expression (n = 4). (B) Representative images of EdU staining and quantification of proliferating cells. bar = 100 μm. (C) Western blot analysis and quantification of MMP2 expression (n=4). (D) Representative images of wound healing assays at 0 h and 24 h, and quantitative analysis of migration rate. bar=100 μm. (E) Western blot analysis and quantification of α-SMA expression (n=4). (F) Representative immunofluorescence staining of α-SMA (green) and DAPI (blue). bar=100 μm. (G) Western blot analysis of PI3K/Akt signaling pathway–related proteins, including phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), and total Akt (n=4). Data are presented as mean ± SEM from at four independent experiments. Statistical significance was determined by one-way ANOVAfollowed by appropriate post hoc tests. bar=100 μm.

    Journal: Frontiers in Pharmacology

    Article Title: SLC7A5 promotes vascular remodeling in the rat carotid artery following balloon injury through PI3K/Akt signaling pathway

    doi: 10.3389/fphar.2026.1857850

    Figure Lengend Snippet: Inhibition of SLC7A5 suppresses PDGF-BB–induced VSMC activation and PI3K/Akt signaling in vitro . (A) Western blot analysis and quantification of PCNA expression (n = 4). (B) Representative images of EdU staining and quantification of proliferating cells. bar = 100 μm. (C) Western blot analysis and quantification of MMP2 expression (n=4). (D) Representative images of wound healing assays at 0 h and 24 h, and quantitative analysis of migration rate. bar=100 μm. (E) Western blot analysis and quantification of α-SMA expression (n=4). (F) Representative immunofluorescence staining of α-SMA (green) and DAPI (blue). bar=100 μm. (G) Western blot analysis of PI3K/Akt signaling pathway–related proteins, including phosphorylated PI3K (p-PI3K), total PI3K, phosphorylated Akt (p-Akt), and total Akt (n=4). Data are presented as mean ± SEM from at four independent experiments. Statistical significance was determined by one-way ANOVAfollowed by appropriate post hoc tests. bar=100 μm.

    Article Snippet: JPH203 (KYT-0353) provided by Targetmol was dissolved in DMSO to prepare stock solution,and PDGF-BB from MCE (HY-P7278) was reconstituted in sterile normal saline according to the manufacturer’s instructions.

    Techniques: Inhibition, Activation Assay, In Vitro, Western Blot, Expressing, Staining, Migration, Immunofluorescence

    Continuous intraosseous administration of SCS prevents glucocorticoid-induced bone degeneration. ( A ) Schematic illustration of the glucocorticoid (GC; MPS)-induced bone deterioration and intraosseous SCS treatment. ( B-D ) Representative H&E staining images of the femur at 6 weeks (B). Magnified views of the cortical bone and trabecular bone in the marrow cavity are shown on the right. Solid arrows indicate normal osteocytes, while hollow arrows indicate empty osteocyte lacunae. Quantification of empty lacunae ratios in cortical bone (C) and trabecular bone (D). n = 6 biological replicates. (Scale bars, 500 μm and 25 μm) ( E-H ) Representative immunofluorescence staining of OPN + mature osteoblasts, osteolectin + osteoprogenitors, and VE-cadherin + endothelial cells (ECs) in femur at 6 weeks (E), and corresponding quantifications (F–H). n = 6 biological replicates. (Scale bars, 100 μm and 20 μm) ( I and J ) Representative flow cytometry plots of capillary subtypes in the femur (I), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (J). n = 6 biological replicates. ( K and L ) Flow cytometry plots showing Sca-1 hi CD31 hi arteriolar ECs (K), and corresponding quantification (L). n = 6 biological replicates. ( M and N ) Representative micro-CT 3D images of the femur (M). Quantitative analysis of percent bone volume (BV/TV) (N). n = 6 biological replicates. (Scale bars, 1.5 mm, 600 μm and 545 μm) ( O and P ) ELISA analysis of VEGF (O) and PDGF-BB (P) levels in bone marrow supernatant and peripheral serum from PBS- and SCS-treated groups at week 6. n = 6 biological replicates. ( Q ) ELISA quantification of the osteogenic factor osteocalcin in peripheral serum at week 6. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, F, G, H, J, L, N, O, P and Q ).

    Journal: Bioactive Materials

    Article Title: Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming

    doi: 10.1016/j.bioactmat.2025.11.039

    Figure Lengend Snippet: Continuous intraosseous administration of SCS prevents glucocorticoid-induced bone degeneration. ( A ) Schematic illustration of the glucocorticoid (GC; MPS)-induced bone deterioration and intraosseous SCS treatment. ( B-D ) Representative H&E staining images of the femur at 6 weeks (B). Magnified views of the cortical bone and trabecular bone in the marrow cavity are shown on the right. Solid arrows indicate normal osteocytes, while hollow arrows indicate empty osteocyte lacunae. Quantification of empty lacunae ratios in cortical bone (C) and trabecular bone (D). n = 6 biological replicates. (Scale bars, 500 μm and 25 μm) ( E-H ) Representative immunofluorescence staining of OPN + mature osteoblasts, osteolectin + osteoprogenitors, and VE-cadherin + endothelial cells (ECs) in femur at 6 weeks (E), and corresponding quantifications (F–H). n = 6 biological replicates. (Scale bars, 100 μm and 20 μm) ( I and J ) Representative flow cytometry plots of capillary subtypes in the femur (I), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (J). n = 6 biological replicates. ( K and L ) Flow cytometry plots showing Sca-1 hi CD31 hi arteriolar ECs (K), and corresponding quantification (L). n = 6 biological replicates. ( M and N ) Representative micro-CT 3D images of the femur (M). Quantitative analysis of percent bone volume (BV/TV) (N). n = 6 biological replicates. (Scale bars, 1.5 mm, 600 μm and 545 μm) ( O and P ) ELISA analysis of VEGF (O) and PDGF-BB (P) levels in bone marrow supernatant and peripheral serum from PBS- and SCS-treated groups at week 6. n = 6 biological replicates. ( Q ) ELISA quantification of the osteogenic factor osteocalcin in peripheral serum at week 6. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, F, G, H, J, L, N, O, P and Q ).

    Article Snippet: Levels of angiogenesis-associated factors, including VEGF (Neobioscience, EMC103.96) and PDGF-BB (R&D Systems, MBB00), were quantified in both bone marrow supernatants and serum using ELISA kits according to the manufacturer's instructions.

    Techniques: Staining, Immunofluorescence, Flow Cytometry, Micro-CT, Enzyme-linked Immunosorbent Assay

    SCS targets downstream senescent lineage commitment of bone marrow MSCs to mitigate GC-induced bone deterioration. ( A ) Schematic diagram illustrating the experimental design: CD45 − Ter119 − CD31 − LepR + MSCs isolated from mice co-treated with SCS and MPS for 7 days were subjected to in vitro lineage-competitive differentiation, followed by DEX-induced senescence in lineage-mixed cells. These cells were then adoptively transplanted into healthy bone marrow cavity to assess bone deterioration development. ( B ) Representative H&E-stained images of the femur 12 weeks after adoptive transfer. PBS-DEX group: LepR + MSCs from PBS and MPS co-treated mice subjected to in vitro lineage differentiation and DEX-induced senescence, followed by transplantation. SCS-DEX group: LepR + MSCs from SCS and MPS co-treated mice processed similarly. PBS group: solvent control without cell transplantation. Solid arrows indicate intact osteocytes; hollow arrows indicate empty lacunae. (Scale bars, 250 μm and 25 μm) ( C – E ) Quantitative analysis of marrow hypertrophic adipocyte diameter (C), proportion of empty osteocyte lacunae in trabecular bone (D), and adipocyte number (E) in the metaphysis 12 weeks post-transplantation. n = 19 biological replicates (C), n = 6 biological replicates (D), n = 8 biological replicates (E). ( F ) Quantification of empty lacunae in epiphysis at 12 weeks post-transplantation. n = 6 biological replicates. ( G – I ) Representative flow cytometry plots of capillary ECs subtypes in the femur at 12 weeks (G), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (H) and CD45 − Ter119 − CD31 lo Emcn lo ECs (I). n = 6 biological replicates. ( J and K ) Representative flow cytometry plots (J) and corresponding quantification (K) of CD45 − Ter119 − Sca-1 hi CD31 hi arteriolar ECs in the femur at 12 weeks post-transplantation. n = 6 biological replicates. ( L ) Representative micro-CT images of the femur at 12 weeks post-transplantation across different treatment groups. (Scale bars, 1.5 mm and 500 μm) ( M – P ) Quantitative analysis of bone parameters in the metaphysis: bone mineral density (BMD) (M), percent bone volume (BV/TV) (N), trabecular separation (Tb.Sp) (O), and trabecular number (Tb.N) (P). n = 6 biological replicates. ( Q ) Serum ELISA analysis of the osteogenic marker osteocalcin at 12 weeks post-transplantation. n = 6 biological replicates. ( R and S ) ELISA analysis of PDGF-BB (R) and VEGF (S) in both bone marrow supernatant and peripheral serum at 12 weeks post-transplantation. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, E, F, H, I, K, M, N, O, P, Q, R and S ).

    Journal: Bioactive Materials

    Article Title: Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming

    doi: 10.1016/j.bioactmat.2025.11.039

    Figure Lengend Snippet: SCS targets downstream senescent lineage commitment of bone marrow MSCs to mitigate GC-induced bone deterioration. ( A ) Schematic diagram illustrating the experimental design: CD45 − Ter119 − CD31 − LepR + MSCs isolated from mice co-treated with SCS and MPS for 7 days were subjected to in vitro lineage-competitive differentiation, followed by DEX-induced senescence in lineage-mixed cells. These cells were then adoptively transplanted into healthy bone marrow cavity to assess bone deterioration development. ( B ) Representative H&E-stained images of the femur 12 weeks after adoptive transfer. PBS-DEX group: LepR + MSCs from PBS and MPS co-treated mice subjected to in vitro lineage differentiation and DEX-induced senescence, followed by transplantation. SCS-DEX group: LepR + MSCs from SCS and MPS co-treated mice processed similarly. PBS group: solvent control without cell transplantation. Solid arrows indicate intact osteocytes; hollow arrows indicate empty lacunae. (Scale bars, 250 μm and 25 μm) ( C – E ) Quantitative analysis of marrow hypertrophic adipocyte diameter (C), proportion of empty osteocyte lacunae in trabecular bone (D), and adipocyte number (E) in the metaphysis 12 weeks post-transplantation. n = 19 biological replicates (C), n = 6 biological replicates (D), n = 8 biological replicates (E). ( F ) Quantification of empty lacunae in epiphysis at 12 weeks post-transplantation. n = 6 biological replicates. ( G – I ) Representative flow cytometry plots of capillary ECs subtypes in the femur at 12 weeks (G), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (H) and CD45 − Ter119 − CD31 lo Emcn lo ECs (I). n = 6 biological replicates. ( J and K ) Representative flow cytometry plots (J) and corresponding quantification (K) of CD45 − Ter119 − Sca-1 hi CD31 hi arteriolar ECs in the femur at 12 weeks post-transplantation. n = 6 biological replicates. ( L ) Representative micro-CT images of the femur at 12 weeks post-transplantation across different treatment groups. (Scale bars, 1.5 mm and 500 μm) ( M – P ) Quantitative analysis of bone parameters in the metaphysis: bone mineral density (BMD) (M), percent bone volume (BV/TV) (N), trabecular separation (Tb.Sp) (O), and trabecular number (Tb.N) (P). n = 6 biological replicates. ( Q ) Serum ELISA analysis of the osteogenic marker osteocalcin at 12 weeks post-transplantation. n = 6 biological replicates. ( R and S ) ELISA analysis of PDGF-BB (R) and VEGF (S) in both bone marrow supernatant and peripheral serum at 12 weeks post-transplantation. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, E, F, H, I, K, M, N, O, P, Q, R and S ).

    Article Snippet: Levels of angiogenesis-associated factors, including VEGF (Neobioscience, EMC103.96) and PDGF-BB (R&D Systems, MBB00), were quantified in both bone marrow supernatants and serum using ELISA kits according to the manufacturer's instructions.

    Techniques: Isolation, In Vitro, Staining, Adoptive Transfer Assay, Transplantation Assay, Solvent, Control, Flow Cytometry, Micro-CT, Enzyme-linked Immunosorbent Assay, Marker