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fgf2 neutralizing antibody  (R&D Systems)


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    Structured Review

    R&D Systems fgf2 neutralizing antibody
    Low density porcine chondrocytes were stimulated with injury CM in the presence or absence of FGFRi (250nM SB402451) or <t>anti-FGF2</t> neutralising antibody (4 μg/mL) and imaged using the IncuCyte imaging system. A , Representative images of cells after 96h culture. B , C , Quantitation of cell density assessed by IncuCyte imaging (at 2h intervals) over 96h. Movie showing change in cell morphology and proliferation for each condition are presented in supplementary video data file S5. D , Yap-Tead GFP reporter assay after stimulation of cells with IL-6/IL-6R (positive control), injury CM at indicated dilutions, with or without FGFRi (250 nM). Graph shows mean ± SD. Data points indicate independent experiments. One-way ANOVA with Tukey’s post-test, n = 6. Quantification E , and representative images F , of in vivo murine cartilage repair model, induced at 10 weeks of age and assessed after 8 weeks, in FGF2 -/- and DBA1 control mice. Histological sections were scored using a modified Pineda score. Mean ± SEM; Mann-Whitney U test; *p>0.05, **p>0.01, n = 12 biological replicates.
    Fgf2 Neutralizing Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 34 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Mechano-activated chondroprogenitors (MACs) drive intrinsic cartilage repair; a process that is arrested in osteoarthritis"

    Article Title: Mechano-activated chondroprogenitors (MACs) drive intrinsic cartilage repair; a process that is arrested in osteoarthritis

    Journal: bioRxiv

    doi: 10.1101/2025.08.21.671507

    Low density porcine chondrocytes were stimulated with injury CM in the presence or absence of FGFRi (250nM SB402451) or anti-FGF2 neutralising antibody (4 μg/mL) and imaged using the IncuCyte imaging system. A , Representative images of cells after 96h culture. B , C , Quantitation of cell density assessed by IncuCyte imaging (at 2h intervals) over 96h. Movie showing change in cell morphology and proliferation for each condition are presented in supplementary video data file S5. D , Yap-Tead GFP reporter assay after stimulation of cells with IL-6/IL-6R (positive control), injury CM at indicated dilutions, with or without FGFRi (250 nM). Graph shows mean ± SD. Data points indicate independent experiments. One-way ANOVA with Tukey’s post-test, n = 6. Quantification E , and representative images F , of in vivo murine cartilage repair model, induced at 10 weeks of age and assessed after 8 weeks, in FGF2 -/- and DBA1 control mice. Histological sections were scored using a modified Pineda score. Mean ± SEM; Mann-Whitney U test; *p>0.05, **p>0.01, n = 12 biological replicates.
    Figure Legend Snippet: Low density porcine chondrocytes were stimulated with injury CM in the presence or absence of FGFRi (250nM SB402451) or anti-FGF2 neutralising antibody (4 μg/mL) and imaged using the IncuCyte imaging system. A , Representative images of cells after 96h culture. B , C , Quantitation of cell density assessed by IncuCyte imaging (at 2h intervals) over 96h. Movie showing change in cell morphology and proliferation for each condition are presented in supplementary video data file S5. D , Yap-Tead GFP reporter assay after stimulation of cells with IL-6/IL-6R (positive control), injury CM at indicated dilutions, with or without FGFRi (250 nM). Graph shows mean ± SD. Data points indicate independent experiments. One-way ANOVA with Tukey’s post-test, n = 6. Quantification E , and representative images F , of in vivo murine cartilage repair model, induced at 10 weeks of age and assessed after 8 weeks, in FGF2 -/- and DBA1 control mice. Histological sections were scored using a modified Pineda score. Mean ± SEM; Mann-Whitney U test; *p>0.05, **p>0.01, n = 12 biological replicates.

    Techniques Used: Imaging, Quantitation Assay, Reporter Assay, Positive Control, In Vivo, Control, Modification, MANN-WHITNEY

    A , Illustration of SJD. B, Volcano plot showing mean difference (log) in protein expression against adjusted p-values, pre and post SJD in paired samples (n = 16, 5471 proteins, padj ≤ 0.05). Top regulated proteins labelled. C, Line plots for a selection of regulated proteins. INHBA, inhibin βA; ACTIVIN A, inhibin βA homodimer; ACTIVIN AC, Inhibin βA:Inhibin βC heterodimer; BMP, bone morphogenetic proteins-5 & 6. SOX-9, SRY box transcription factor-9; COL2A1, collagen type II a1 chain; COL10A1, collagen type 10 a1 chain; HPLN1, link protein; HSPG2, perlecan. D , Top 10 pathways after gene enrichment analysis (Reactome). E , Cell confluency by IncuCyte imaging of primary chondrocytes stimulated with injury CM in the presence of anti-activin A. F , Chondrogenesis assay of MACs (generated by 72h treatment with injury CM) in the presence of recombinant FGF2 or activin A. Expression of chondrogenic marker genes measured by qPCR at day 3. G , Schematic of the intrinsic repair cycle of articular cartilage. A and G created using BioRender.
    Figure Legend Snippet: A , Illustration of SJD. B, Volcano plot showing mean difference (log) in protein expression against adjusted p-values, pre and post SJD in paired samples (n = 16, 5471 proteins, padj ≤ 0.05). Top regulated proteins labelled. C, Line plots for a selection of regulated proteins. INHBA, inhibin βA; ACTIVIN A, inhibin βA homodimer; ACTIVIN AC, Inhibin βA:Inhibin βC heterodimer; BMP, bone morphogenetic proteins-5 & 6. SOX-9, SRY box transcription factor-9; COL2A1, collagen type II a1 chain; COL10A1, collagen type 10 a1 chain; HPLN1, link protein; HSPG2, perlecan. D , Top 10 pathways after gene enrichment analysis (Reactome). E , Cell confluency by IncuCyte imaging of primary chondrocytes stimulated with injury CM in the presence of anti-activin A. F , Chondrogenesis assay of MACs (generated by 72h treatment with injury CM) in the presence of recombinant FGF2 or activin A. Expression of chondrogenic marker genes measured by qPCR at day 3. G , Schematic of the intrinsic repair cycle of articular cartilage. A and G created using BioRender.

    Techniques Used: Expressing, Selection, Imaging, Generated, Recombinant, Marker



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    Low density porcine chondrocytes were stimulated with injury CM in the presence or absence of FGFRi (250nM SB402451) or <t>anti-FGF2</t> neutralising antibody (4 μg/mL) and imaged using the IncuCyte imaging system. A , Representative images of cells after 96h culture. B , C , Quantitation of cell density assessed by IncuCyte imaging (at 2h intervals) over 96h. Movie showing change in cell morphology and proliferation for each condition are presented in supplementary video data file S5. D , Yap-Tead GFP reporter assay after stimulation of cells with IL-6/IL-6R (positive control), injury CM at indicated dilutions, with or without FGFRi (250 nM). Graph shows mean ± SD. Data points indicate independent experiments. One-way ANOVA with Tukey’s post-test, n = 6. Quantification E , and representative images F , of in vivo murine cartilage repair model, induced at 10 weeks of age and assessed after 8 weeks, in FGF2 -/- and DBA1 control mice. Histological sections were scored using a modified Pineda score. Mean ± SEM; Mann-Whitney U test; *p>0.05, **p>0.01, n = 12 biological replicates.
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    ( A , B ) The exogenous <t>FGF2</t> activates VEGFR signaling in GIST T-1 cells via up-regulation of VEGF-A. ( A ) FGF-2 stimulates, whereas <t>anti-FGF2</t> <t>neutralizing</t> Abs abrogates VEGFR signaling GIST T-1 cells. Cells were treated with FGF2 (100 ng/mL), IM (0.02 µM) alone or in the presence of anti-FGF2 neutralizing Abs (20 µg/mL) for 72 h. Expression of VEGF-A, total and phosphorylated forms of VEGFR, KIT, MAPK, AKT, and STAT1 was assessed by immunoblot analysis. Actin stain was used as a loading control for each sample. ( B ) Concentration of VEGF-A (pg/mL, measured by ELISA) in supernatants of IM-naive (GIST T-1) cells treated with DMSO (control), FGF-2 (100 ng/mL), IM (0.02 µM) alone or in the presence of anti-FGF-2 Abs (20 µg/mL) for 72 h. Data are presented as median ± SD. Significant differences with p < 0.05 (*), p < 0.01 (**) from n ≥ 3 using unpaired Student’s t -test. ( C ) Changes in the relative expression level of mRNA VEGF-A and VEGFR1, 2, and 3 in GIST T-1 after treatment with FGF-2 (100 ng/mL), as determined by quantitative RT-PCR. The amplification of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used for internal control. Data are presented as median ± SD. Significant differences with p < 0.05 (*) from n ≥ 3 using unpaired Student’s t -test. The original Western blot figures can be found in .
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    Image Search Results


    Low density porcine chondrocytes were stimulated with injury CM in the presence or absence of FGFRi (250nM SB402451) or anti-FGF2 neutralising antibody (4 μg/mL) and imaged using the IncuCyte imaging system. A , Representative images of cells after 96h culture. B , C , Quantitation of cell density assessed by IncuCyte imaging (at 2h intervals) over 96h. Movie showing change in cell morphology and proliferation for each condition are presented in supplementary video data file S5. D , Yap-Tead GFP reporter assay after stimulation of cells with IL-6/IL-6R (positive control), injury CM at indicated dilutions, with or without FGFRi (250 nM). Graph shows mean ± SD. Data points indicate independent experiments. One-way ANOVA with Tukey’s post-test, n = 6. Quantification E , and representative images F , of in vivo murine cartilage repair model, induced at 10 weeks of age and assessed after 8 weeks, in FGF2 -/- and DBA1 control mice. Histological sections were scored using a modified Pineda score. Mean ± SEM; Mann-Whitney U test; *p>0.05, **p>0.01, n = 12 biological replicates.

    Journal: bioRxiv

    Article Title: Mechano-activated chondroprogenitors (MACs) drive intrinsic cartilage repair; a process that is arrested in osteoarthritis

    doi: 10.1101/2025.08.21.671507

    Figure Lengend Snippet: Low density porcine chondrocytes were stimulated with injury CM in the presence or absence of FGFRi (250nM SB402451) or anti-FGF2 neutralising antibody (4 μg/mL) and imaged using the IncuCyte imaging system. A , Representative images of cells after 96h culture. B , C , Quantitation of cell density assessed by IncuCyte imaging (at 2h intervals) over 96h. Movie showing change in cell morphology and proliferation for each condition are presented in supplementary video data file S5. D , Yap-Tead GFP reporter assay after stimulation of cells with IL-6/IL-6R (positive control), injury CM at indicated dilutions, with or without FGFRi (250 nM). Graph shows mean ± SD. Data points indicate independent experiments. One-way ANOVA with Tukey’s post-test, n = 6. Quantification E , and representative images F , of in vivo murine cartilage repair model, induced at 10 weeks of age and assessed after 8 weeks, in FGF2 -/- and DBA1 control mice. Histological sections were scored using a modified Pineda score. Mean ± SEM; Mann-Whitney U test; *p>0.05, **p>0.01, n = 12 biological replicates.

    Article Snippet: Human recombinant FGF2 was purchased from Peprotech EC Ltd. Recombinant human Activin A (MAB3381), TGF-βR3 (QK054), FGF2 neutralizing antibody (AF-233-NA) and Activin A neutralizing antibody (MAB3381) were obtained from R&D Systems.

    Techniques: Imaging, Quantitation Assay, Reporter Assay, Positive Control, In Vivo, Control, Modification, MANN-WHITNEY

    A , Illustration of SJD. B, Volcano plot showing mean difference (log) in protein expression against adjusted p-values, pre and post SJD in paired samples (n = 16, 5471 proteins, padj ≤ 0.05). Top regulated proteins labelled. C, Line plots for a selection of regulated proteins. INHBA, inhibin βA; ACTIVIN A, inhibin βA homodimer; ACTIVIN AC, Inhibin βA:Inhibin βC heterodimer; BMP, bone morphogenetic proteins-5 & 6. SOX-9, SRY box transcription factor-9; COL2A1, collagen type II a1 chain; COL10A1, collagen type 10 a1 chain; HPLN1, link protein; HSPG2, perlecan. D , Top 10 pathways after gene enrichment analysis (Reactome). E , Cell confluency by IncuCyte imaging of primary chondrocytes stimulated with injury CM in the presence of anti-activin A. F , Chondrogenesis assay of MACs (generated by 72h treatment with injury CM) in the presence of recombinant FGF2 or activin A. Expression of chondrogenic marker genes measured by qPCR at day 3. G , Schematic of the intrinsic repair cycle of articular cartilage. A and G created using BioRender.

    Journal: bioRxiv

    Article Title: Mechano-activated chondroprogenitors (MACs) drive intrinsic cartilage repair; a process that is arrested in osteoarthritis

    doi: 10.1101/2025.08.21.671507

    Figure Lengend Snippet: A , Illustration of SJD. B, Volcano plot showing mean difference (log) in protein expression against adjusted p-values, pre and post SJD in paired samples (n = 16, 5471 proteins, padj ≤ 0.05). Top regulated proteins labelled. C, Line plots for a selection of regulated proteins. INHBA, inhibin βA; ACTIVIN A, inhibin βA homodimer; ACTIVIN AC, Inhibin βA:Inhibin βC heterodimer; BMP, bone morphogenetic proteins-5 & 6. SOX-9, SRY box transcription factor-9; COL2A1, collagen type II a1 chain; COL10A1, collagen type 10 a1 chain; HPLN1, link protein; HSPG2, perlecan. D , Top 10 pathways after gene enrichment analysis (Reactome). E , Cell confluency by IncuCyte imaging of primary chondrocytes stimulated with injury CM in the presence of anti-activin A. F , Chondrogenesis assay of MACs (generated by 72h treatment with injury CM) in the presence of recombinant FGF2 or activin A. Expression of chondrogenic marker genes measured by qPCR at day 3. G , Schematic of the intrinsic repair cycle of articular cartilage. A and G created using BioRender.

    Article Snippet: Human recombinant FGF2 was purchased from Peprotech EC Ltd. Recombinant human Activin A (MAB3381), TGF-βR3 (QK054), FGF2 neutralizing antibody (AF-233-NA) and Activin A neutralizing antibody (MAB3381) were obtained from R&D Systems.

    Techniques: Expressing, Selection, Imaging, Generated, Recombinant, Marker

    ( A , B ) The exogenous FGF2 activates VEGFR signaling in GIST T-1 cells via up-regulation of VEGF-A. ( A ) FGF-2 stimulates, whereas anti-FGF2 neutralizing Abs abrogates VEGFR signaling GIST T-1 cells. Cells were treated with FGF2 (100 ng/mL), IM (0.02 µM) alone or in the presence of anti-FGF2 neutralizing Abs (20 µg/mL) for 72 h. Expression of VEGF-A, total and phosphorylated forms of VEGFR, KIT, MAPK, AKT, and STAT1 was assessed by immunoblot analysis. Actin stain was used as a loading control for each sample. ( B ) Concentration of VEGF-A (pg/mL, measured by ELISA) in supernatants of IM-naive (GIST T-1) cells treated with DMSO (control), FGF-2 (100 ng/mL), IM (0.02 µM) alone or in the presence of anti-FGF-2 Abs (20 µg/mL) for 72 h. Data are presented as median ± SD. Significant differences with p < 0.05 (*), p < 0.01 (**) from n ≥ 3 using unpaired Student’s t -test. ( C ) Changes in the relative expression level of mRNA VEGF-A and VEGFR1, 2, and 3 in GIST T-1 after treatment with FGF-2 (100 ng/mL), as determined by quantitative RT-PCR. The amplification of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used for internal control. Data are presented as median ± SD. Significant differences with p < 0.05 (*) from n ≥ 3 using unpaired Student’s t -test. The original Western blot figures can be found in .

    Journal: Cancers

    Article Title: Fibroblast Growth Factor 2 (FGF2) Activates Vascular Endothelial Growth Factor (VEGF) Signaling in Gastrointestinal Stromal Tumors (GIST): An Autocrine Mechanism Contributing to Imatinib Mesylate (IM) Resistance

    doi: 10.3390/cancers16173103

    Figure Lengend Snippet: ( A , B ) The exogenous FGF2 activates VEGFR signaling in GIST T-1 cells via up-regulation of VEGF-A. ( A ) FGF-2 stimulates, whereas anti-FGF2 neutralizing Abs abrogates VEGFR signaling GIST T-1 cells. Cells were treated with FGF2 (100 ng/mL), IM (0.02 µM) alone or in the presence of anti-FGF2 neutralizing Abs (20 µg/mL) for 72 h. Expression of VEGF-A, total and phosphorylated forms of VEGFR, KIT, MAPK, AKT, and STAT1 was assessed by immunoblot analysis. Actin stain was used as a loading control for each sample. ( B ) Concentration of VEGF-A (pg/mL, measured by ELISA) in supernatants of IM-naive (GIST T-1) cells treated with DMSO (control), FGF-2 (100 ng/mL), IM (0.02 µM) alone or in the presence of anti-FGF-2 Abs (20 µg/mL) for 72 h. Data are presented as median ± SD. Significant differences with p < 0.05 (*), p < 0.01 (**) from n ≥ 3 using unpaired Student’s t -test. ( C ) Changes in the relative expression level of mRNA VEGF-A and VEGFR1, 2, and 3 in GIST T-1 after treatment with FGF-2 (100 ng/mL), as determined by quantitative RT-PCR. The amplification of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used for internal control. Data are presented as median ± SD. Significant differences with p < 0.05 (*) from n ≥ 3 using unpaired Student’s t -test. The original Western blot figures can be found in .

    Article Snippet: Neutralizing antibody against bFGF (Anti-FGF2/basic FGF #05-117) and human recombinant FGF-2/basic (FGF2 #01-106) were from Merck KGaA (Darmstadt, Germany).

    Techniques: Expressing, Western Blot, Staining, Control, Concentration Assay, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Amplification