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R&D Systems recombinant mouse fgf23

( a ) Treatment of neonatal rat ventricular myocyte cardiobundles with fibroblast growth factor (FGF) 23 for 20 minutes significantly increased contractile force, whereas 7 days of chronic treatment led to a significant reduction in contractile force that could be rescued by coapplication of BLU9931, a selective FGFR4 inhibitor. ( b ) Electrophysiological function was evaluated by pacing of cardiobundles and application of Di-4-ANEPPS (6-[2-(N,N-Dibutylamino)naphthyl]ethenyl-4′-pyridinium propanesulfonate) as voltage-sensitive dye. Chronic exposure of cardiobundles to <t>FGF23</t> lead to significantly longer action potential durations. ( c ) FGF23-treated bundles exhibited significantly lower conduction velocity that was normalized after coapplication of BLU9931. Besides functional changes, chronic FGF23 treatment also led to cardiobundle hypertrophy, indicated by the ( d,g ) significant increase in cross-section and ( e ) increased expression of hypertrophic mRNA markers Rcan1 and Trpc6 . Increased expression of Rcan1 and Trpc6 was blocked by parallel treatment with BLU9931. ( f ) Metabolic transcription factors that were increased in chronic kidney disease mice also increased in cardiobundles after FGF23 treatment. ( g ) Representative images of cardiobundles indicate cellular hypertrophy after FGF23 treatment by increased myocyte cross-sections. Bars = 10 μm. ( h ) Gene set enrichment analysis of control and FGF23-treated cardiobundles showed an enrichment of metabolic pathways, particularly fatty acid metabolism, adipogenesis, and cholesterol homeostasis. ( i ) Additional enrichment was detected in pathways related to mitochondrial function, such as oxidative phosphorylation, respiratory chain, organelle fission, and organelle inner membrane. Downregulated pathways after FGF23 treatment include angiogenesis, vascular development, tumor necrosis factor (TNF)-α signaling, and P53. Bar graphs represent mean ± SEM with individual values included in the graph. n ≥ 3 for all experiments. * P < 0.05, ** P < 0.005, **** P < 0.0001. APD, action potential duration; DAPI, 4′,6-diamidino-2-phenylindole; ES, enrichment score; FDR, false discovery rate; NES, normalized enrichment score. To optimize viewing of this image, please see the online version of this article at www.kidney-international.org .

Recombinant Mouse Fgf23, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 21 article reviews

recombinant mouse fgf23 - by Bioz Stars, 2026-09

93/100 stars

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1) Product Images from "Fibroblast growth factor 23 and fibroblast growth factor receptor 4 promote cardiac metabolic remodeling in chronic kidney disease"

Article Title: Fibroblast growth factor 23 and fibroblast growth factor receptor 4 promote cardiac metabolic remodeling in chronic kidney disease

Journal: Kidney international

doi: 10.1016/j.kint.2025.01.024

Figure Legend Snippet: ( a ) Treatment of neonatal rat ventricular myocyte cardiobundles with fibroblast growth factor (FGF) 23 for 20 minutes significantly increased contractile force, whereas 7 days of chronic treatment led to a significant reduction in contractile force that could be rescued by coapplication of BLU9931, a selective FGFR4 inhibitor. ( b ) Electrophysiological function was evaluated by pacing of cardiobundles and application of Di-4-ANEPPS (6-[2-(N,N-Dibutylamino)naphthyl]ethenyl-4′-pyridinium propanesulfonate) as voltage-sensitive dye. Chronic exposure of cardiobundles to FGF23 lead to significantly longer action potential durations. ( c ) FGF23-treated bundles exhibited significantly lower conduction velocity that was normalized after coapplication of BLU9931. Besides functional changes, chronic FGF23 treatment also led to cardiobundle hypertrophy, indicated by the ( d,g ) significant increase in cross-section and ( e ) increased expression of hypertrophic mRNA markers Rcan1 and Trpc6 . Increased expression of Rcan1 and Trpc6 was blocked by parallel treatment with BLU9931. ( f ) Metabolic transcription factors that were increased in chronic kidney disease mice also increased in cardiobundles after FGF23 treatment. ( g ) Representative images of cardiobundles indicate cellular hypertrophy after FGF23 treatment by increased myocyte cross-sections. Bars = 10 μm. ( h ) Gene set enrichment analysis of control and FGF23-treated cardiobundles showed an enrichment of metabolic pathways, particularly fatty acid metabolism, adipogenesis, and cholesterol homeostasis. ( i ) Additional enrichment was detected in pathways related to mitochondrial function, such as oxidative phosphorylation, respiratory chain, organelle fission, and organelle inner membrane. Downregulated pathways after FGF23 treatment include angiogenesis, vascular development, tumor necrosis factor (TNF)-α signaling, and P53. Bar graphs represent mean ± SEM with individual values included in the graph. n ≥ 3 for all experiments. * P < 0.05, ** P < 0.005, **** P < 0.0001. APD, action potential duration; DAPI, 4′,6-diamidino-2-phenylindole; ES, enrichment score; FDR, false discovery rate; NES, normalized enrichment score. To optimize viewing of this image, please see the online version of this article at www.kidney-international.org .

Techniques Used: Functional Assay, Expressing, Control, Phospho-proteomics, Membrane

( a,b ) Cultured neonatal rat ventricular myocytes (NRVMs) responded to 48 hours of fibroblast growth factor (FGF) 23 treatment with significant hypertrophy, indicated by increased cross-sectional area and expression of prohypertrophic markers. Prohypertrophic mRNA expression and cellular hypertrophy could be mitigated by parallel treatment with the FGFR4-specific inhibitor BLU9931. ( a ) Bar = 30 μm. ( c ) NRVMs treated with FGF23 for 1 hour, before observable hypertrophy takes place, were analyzed in a Seahorse XF analyzer for extracellular acidification rate (ECAR), elevated total proton efflux rates (PERs), and glycolysis-specific PER (GlycoPER). ECAR was significantly higher in FGF23-treated cells, which could be reduced to control levels by BLU9931. PER showed elevated basal and compensatory glycolysis on FGF23 treatment; glycolysis-specific proton efflux was also increased. These FGF23-mediated effects were blocked by BLU9931 application. ( c ) Graphs represent 3 independent experiments. ( d ) Seahorse mitochondrial stress test assay showed increased basal and maximal mitochondrial respiration after FGF23 treatment of NRVMs. Adenosine triphosphate (ATP) production-linked, spare respiratory capacity and nonmitochondrial oxygen consumption rate increased in parallel after FGF23 treatment. The significant decrease in coupling efficiency and the increased proton leak indicate uncoupling of substrate oxidation and ATP synthesis after 1 hour of FGF23 treatment. Application of BLU9931 or the calcineurin inhibitor, cyclosporin A, prevented the changes to mitochondrial function caused by FGF23. Bar graphs represent mean ± SEM and individual values included in the graph. n ≥ 9 for all experiments. * P < 0.05, ** P < 0.005, **** P < 0.0001. DMSO, dimethylsulfoxide; Max, maximum; NS, not significant; PBS, phosphate-buffered saline. To optimize viewing of this image, please see the online version of this article at www.kidney-international.org .

Figure Legend Snippet: ( a,b ) Cultured neonatal rat ventricular myocytes (NRVMs) responded to 48 hours of fibroblast growth factor (FGF) 23 treatment with significant hypertrophy, indicated by increased cross-sectional area and expression of prohypertrophic markers. Prohypertrophic mRNA expression and cellular hypertrophy could be mitigated by parallel treatment with the FGFR4-specific inhibitor BLU9931. ( a ) Bar = 30 μm. ( c ) NRVMs treated with FGF23 for 1 hour, before observable hypertrophy takes place, were analyzed in a Seahorse XF analyzer for extracellular acidification rate (ECAR), elevated total proton efflux rates (PERs), and glycolysis-specific PER (GlycoPER). ECAR was significantly higher in FGF23-treated cells, which could be reduced to control levels by BLU9931. PER showed elevated basal and compensatory glycolysis on FGF23 treatment; glycolysis-specific proton efflux was also increased. These FGF23-mediated effects were blocked by BLU9931 application. ( c ) Graphs represent 3 independent experiments. ( d ) Seahorse mitochondrial stress test assay showed increased basal and maximal mitochondrial respiration after FGF23 treatment of NRVMs. Adenosine triphosphate (ATP) production-linked, spare respiratory capacity and nonmitochondrial oxygen consumption rate increased in parallel after FGF23 treatment. The significant decrease in coupling efficiency and the increased proton leak indicate uncoupling of substrate oxidation and ATP synthesis after 1 hour of FGF23 treatment. Application of BLU9931 or the calcineurin inhibitor, cyclosporin A, prevented the changes to mitochondrial function caused by FGF23. Bar graphs represent mean ± SEM and individual values included in the graph. n ≥ 9 for all experiments. * P < 0.05, ** P < 0.005, **** P < 0.0001. DMSO, dimethylsulfoxide; Max, maximum; NS, not significant; PBS, phosphate-buffered saline. To optimize viewing of this image, please see the online version of this article at www.kidney-international.org .

Techniques Used: Cell Culture, Expressing, Control, Saline

Recombinant:

Article Title: Fibroblast Growth Factor 23 Stimulates Cardiac Fibroblast Activity through Phospholipase C-Mediated Calcium Signaling.
Article Snippet: .. Cardiac fibroblasts treated without and with recombinant mouse FGF-23 (1, 5 or 25 ng/mL; R&D Systems, Abingdon, UK) in the presence and absence of an FGF receptor 1 antagonist (PD166866, 1 μM; Sigma, St. Louis, MO, USA), a free Ca2+ chelator (EGTA, 1 mM; Sigma), or a PLC inhibitor (U73122, 1 μM; Abcam, Cambridge, UK) for 48 h were harvested for further analysis. .. The proliferation of cardiac fibroblasts was determined using a commercial MTS kit (Promega, Madison, WI), as described previously [23].

Article Title: A protective role for FGF-23 in local defence against disrupted arterial wall integrity?
Article Snippet: .. Recombinant mouse FGF-23 and Klotho were used as positive controls (R&D Systems). .. Nitrocellulose membranes were probed overnight at 4°C with anti-FGF-23 (R&D Systems), anti-Klotho (Abcam, Cambridge, UK), anti-FGFR1 (Cell Signaling Technology, Beverly, MA, USA) or anti-cleaved caspase 3 primary antibody (Cell Signaling Technology), washed in TBST and incubated with goat anti-rat (FGF-23) or goat anti-rabbit (Klotho, cleaved caspase-3 and FGFR1) IgG peroxidase secondary antibody (DAKO, Glostrup, Denmark) for 1h (1:3000 dilution in 5% BSA).

Article Title: A protective role for FGF-23 in local defence against disrupted arterial wall integrity?
Article Snippet: .. Recombinant mouse FGF-23 (R&D Systems, Abingdon, UK) at 10–50 ng/ml was added to cultures at confluence for up to 9 days. .. PD98059 (Sigma) at 10 μM and PD173074 (Source Bioscience, Nottingham, UK) at 10 and 50nM were also added at confluence in 0.1% DMSO to inhibit Erk1/2 signalling and FGFR1, respectively.

Article Title: Fibroblast growth factor 9 (FGF9) inhibits myogenic differentiation of C2C12 and human muscle cells
Article Snippet: CellTiter 96® AQueous One kit and recombinant human basic FGF were obtained from Promega (Madison, WI, USA). .. Recombinant Mouse FGF-9, Recombinant Human FGF-9, Recombinant Mouse FGF-23, Recombinant Human FGF-16, and Recombinant Human FGF-20 were from R&D Systems Inc. (Minneapolis, MN, USA). .. C2C12 cells were obtained from American Type Culture Collection (ATCC) (Manassas, VA, USA).

Article Title: FGF-23 dysregulates calcium homeostasis and electrophysiological properties in HL-1 atrial cells.
Article Snippet: Background Fibroblast growth factor (FGF)-23 is a key regulator of phosphate homeostasis.. Higher FGF-23 levels are correlated with poor outcomes in cardiovascular diseases.. FGF-23 can produce cardiac hypertrophy and increase intracellular calcium, which can change cardiac electrical activity.

Article Title: Fibroblast Growth Factor 23 Stimulates Cardiac Fibroblast Activity through Phospholipase C-Mediated Calcium Signaling
Article Snippet: .. Cardiac fibroblasts treated without and with recombinant mouse FGF-23 (1, 5 or 25 ng/mL; R&D Systems, Abingdon, UK) in the presence and absence of an FGF receptor 1 antagonist (PD166866, 1 μM; Sigma, St. Louis, MO, USA), a free Ca 2+ chelator (EGTA, 1 mM; Sigma), or a PLC inhibitor (U73122, 1 μM; Abcam, Cambridge, UK) for 48 h were harvested for further analysis. .. The proliferation of cardiac fibroblasts was determined using a commercial MTS kit (Promega, Madison, WI), as described previously [ ].

Article Title: Fibroblast growth factor-23 promotes rhythm alterations and contractile dysfunction in adult ventricular cardiomyocytes.
Article Snippet: Background.. Cardiac dysfunction and arrhythmia are common and onerous cardiovascular events in end-stage renal disease (ESRD) patients, especially those on dialysis.. Fibroblast growth factor (FGF)-23 is a phosphate-regulating hormone whose levels dramatically increase as renal function declines.

Planar Chromatography:

Image Search Results

Journal: Kidney international

Article Title: Fibroblast growth factor 23 and fibroblast growth factor receptor 4 promote cardiac metabolic remodeling in chronic kidney disease

doi: 10.1016/j.kint.2025.01.024

Figure Lengend Snippet: ( a ) Treatment of neonatal rat ventricular myocyte cardiobundles with fibroblast growth factor (FGF) 23 for 20 minutes significantly increased contractile force, whereas 7 days of chronic treatment led to a significant reduction in contractile force that could be rescued by coapplication of BLU9931, a selective FGFR4 inhibitor. ( b ) Electrophysiological function was evaluated by pacing of cardiobundles and application of Di-4-ANEPPS (6-[2-(N,N-Dibutylamino)naphthyl]ethenyl-4′-pyridinium propanesulfonate) as voltage-sensitive dye. Chronic exposure of cardiobundles to FGF23 lead to significantly longer action potential durations. ( c ) FGF23-treated bundles exhibited significantly lower conduction velocity that was normalized after coapplication of BLU9931. Besides functional changes, chronic FGF23 treatment also led to cardiobundle hypertrophy, indicated by the ( d,g ) significant increase in cross-section and ( e ) increased expression of hypertrophic mRNA markers Rcan1 and Trpc6 . Increased expression of Rcan1 and Trpc6 was blocked by parallel treatment with BLU9931. ( f ) Metabolic transcription factors that were increased in chronic kidney disease mice also increased in cardiobundles after FGF23 treatment. ( g ) Representative images of cardiobundles indicate cellular hypertrophy after FGF23 treatment by increased myocyte cross-sections. Bars = 10 μm. ( h ) Gene set enrichment analysis of control and FGF23-treated cardiobundles showed an enrichment of metabolic pathways, particularly fatty acid metabolism, adipogenesis, and cholesterol homeostasis. ( i ) Additional enrichment was detected in pathways related to mitochondrial function, such as oxidative phosphorylation, respiratory chain, organelle fission, and organelle inner membrane. Downregulated pathways after FGF23 treatment include angiogenesis, vascular development, tumor necrosis factor (TNF)-α signaling, and P53. Bar graphs represent mean ± SEM with individual values included in the graph. n ≥ 3 for all experiments. * P < 0.05, ** P < 0.005, **** P < 0.0001. APD, action potential duration; DAPI, 4′,6-diamidino-2-phenylindole; ES, enrichment score; FDR, false discovery rate; NES, normalized enrichment score. To optimize viewing of this image, please see the online version of this article at www.kidney-international.org .

Article Snippet: Carrier-free recombinant mouse FGF23 (catalog number 2629-FG025/CF, R&D Systems) was used at 25 and 100 ng/ml.

Techniques: Functional Assay, Expressing, Control, Phospho-proteomics, Membrane

Journal: Kidney international

Article Title: Fibroblast growth factor 23 and fibroblast growth factor receptor 4 promote cardiac metabolic remodeling in chronic kidney disease

doi: 10.1016/j.kint.2025.01.024

Figure Lengend Snippet: ( a,b ) Cultured neonatal rat ventricular myocytes (NRVMs) responded to 48 hours of fibroblast growth factor (FGF) 23 treatment with significant hypertrophy, indicated by increased cross-sectional area and expression of prohypertrophic markers. Prohypertrophic mRNA expression and cellular hypertrophy could be mitigated by parallel treatment with the FGFR4-specific inhibitor BLU9931. ( a ) Bar = 30 μm. ( c ) NRVMs treated with FGF23 for 1 hour, before observable hypertrophy takes place, were analyzed in a Seahorse XF analyzer for extracellular acidification rate (ECAR), elevated total proton efflux rates (PERs), and glycolysis-specific PER (GlycoPER). ECAR was significantly higher in FGF23-treated cells, which could be reduced to control levels by BLU9931. PER showed elevated basal and compensatory glycolysis on FGF23 treatment; glycolysis-specific proton efflux was also increased. These FGF23-mediated effects were blocked by BLU9931 application. ( c ) Graphs represent 3 independent experiments. ( d ) Seahorse mitochondrial stress test assay showed increased basal and maximal mitochondrial respiration after FGF23 treatment of NRVMs. Adenosine triphosphate (ATP) production-linked, spare respiratory capacity and nonmitochondrial oxygen consumption rate increased in parallel after FGF23 treatment. The significant decrease in coupling efficiency and the increased proton leak indicate uncoupling of substrate oxidation and ATP synthesis after 1 hour of FGF23 treatment. Application of BLU9931 or the calcineurin inhibitor, cyclosporin A, prevented the changes to mitochondrial function caused by FGF23. Bar graphs represent mean ± SEM and individual values included in the graph. n ≥ 9 for all experiments. * P < 0.05, ** P < 0.005, **** P < 0.0001. DMSO, dimethylsulfoxide; Max, maximum; NS, not significant; PBS, phosphate-buffered saline. To optimize viewing of this image, please see the online version of this article at www.kidney-international.org .

Article Snippet: Carrier-free recombinant mouse FGF23 (catalog number 2629-FG025/CF, R&D Systems) was used at 25 and 100 ng/ml.

Techniques: Cell Culture, Expressing, Control, Saline

$Figure 1. Dietary phosphate supplementation aggravates FGF23 excess and bone microarchitecture in Dmp1KO mice. Serum levels of (A) total FGF23 (cFGF23), (B) intact FGF23 (iFGF23), (C) intact to total FGF23 ratio (i/c FGF23), (D) parathyroid hormone (PTH), (E) 1,25-dihydroxyvitamin D [1,25(OH)2D], (F) calcium (Ca2+), and (G) phosphate (Pi); (H) fractional excretion of Pi (FePi); (I) body weight, (J) tail length, and (K) femur length; 3D-μCT scan reconstruction of (L) distal femur trabecular metaphysis (scale bar = 200 μm); (M) midshaft femur cortical diaphysis (scale bar = 500 μm); (N) 2D μCT analysis of cortical bone porosity (scale bar = 100 μm); (O) red fluorescence microscopy imaging of alizarin red S–stained (ARS-stained) mineralization fronts; (P) bright-field microscopy imaging of modified trichrome Goldner staining; and (Q) tartrate-resistant acidic phosphatase (TRAcP) staining of longitudinal histology sections of distal femur (scale bar = 100 μm for ARS, 500 μm for Goldner and TRAcP). All analyses were performed in 12-week-old WT (n ≥ 5) and Dmp1KO (n ≥ 5) mice fed a diet containing 0.7% Pi (normal Pi, NP) or 2% Pi (high Pi, HP) from 6 to 12 weeks of age. Values are expressed as mean ± SEM; P < 0.05 vs. aNP-WT, bHP-WT, cNP-Dmp1KO; P < 0.1 vs. dNP-WT, eHP-WT. Statistical tests were ANOVA test followed by post hoc t tests and multiple-testing correction using Holm-Bonferroni method.$

Journal: JCI insight

Article Title: FGF23 directly inhibits osteoprogenitor differentiation in Dmp1-knockout mice.

doi: 10.1172/jci.insight.156850

Figure Lengend Snippet: Figure 1. Dietary phosphate supplementation aggravates FGF23 excess and bone microarchitecture in Dmp1KO mice. Serum levels of (A) total FGF23 (cFGF23), (B) intact FGF23 (iFGF23), (C) intact to total FGF23 ratio (i/c FGF23), (D) parathyroid hormone (PTH), (E) 1,25-dihydroxyvitamin D [1,25(OH)2D], (F) calcium (Ca2+), and (G) phosphate (Pi); (H) fractional excretion of Pi (FePi); (I) body weight, (J) tail length, and (K) femur length; 3D-μCT scan reconstruction of (L) distal femur trabecular metaphysis (scale bar = 200 μm); (M) midshaft femur cortical diaphysis (scale bar = 500 μm); (N) 2D μCT analysis of cortical bone porosity (scale bar = 100 μm); (O) red fluorescence microscopy imaging of alizarin red S–stained (ARS-stained) mineralization fronts; (P) bright-field microscopy imaging of modified trichrome Goldner staining; and (Q) tartrate-resistant acidic phosphatase (TRAcP) staining of longitudinal histology sections of distal femur (scale bar = 100 μm for ARS, 500 μm for Goldner and TRAcP). All analyses were performed in 12-week-old WT (n ≥ 5) and Dmp1KO (n ≥ 5) mice fed a diet containing 0.7% Pi (normal Pi, NP) or 2% Pi (high Pi, HP) from 6 to 12 weeks of age. Values are expressed as mean ± SEM; P < 0.05 vs. aNP-WT, bHP-WT, cNP-Dmp1KO; P < 0.1 vs. dNP-WT, eHP-WT. Statistical tests were ANOVA test followed by post hoc t tests and multiple-testing correction using Holm-Bonferroni method.

Article Snippet: We cultured MC3T3-E1 (Subclone 4, CRL-2593, ATCC) osteoblasts for 21 days in osteoblast differentiation medium of similar composition containing 10 mmol/L bGP and 0/25/50 ng/mL of mouse recombinant FGF23 (R&D Systems).

Techniques: Fluorescence, Microscopy, Imaging, Staining, Modification

$Figure 2. Osteocyte-specific deletion of Fgf23 fully corrects hypophosphatemia in Dmp1KO mice. Serum levels of (A) total FGF23 (cFGF23), (B) intact FGF23 (iFGF23), (C) intact to total FGF23 ratio (i/c FGF23), (D) parathyroid hormone (PTH), (E) 1,25-dihydroxyvitamin D [1,25(OH)2D], (F) calcium (Ca2+), and (G) phosphate (Pi); (H) fractional excretion of Pi (FePi); and kidney mRNA expression of (I) NaPi2a, (J) Cyp27b1, and (K) Cyp24a1 in 12-week-old WT (n ≥ 5), Fgf23Dmp1-cKO (n ≥ 5), Dmp1KO (n ≥ 3), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 5) mice. Values are expressed as mean ± SEM; P < 0.05 vs. aWT,$

Journal: JCI insight

Article Title: FGF23 directly inhibits osteoprogenitor differentiation in Dmp1-knockout mice.

doi: 10.1172/jci.insight.156850

Figure Lengend Snippet: Figure 2. Osteocyte-specific deletion of Fgf23 fully corrects hypophosphatemia in Dmp1KO mice. Serum levels of (A) total FGF23 (cFGF23), (B) intact FGF23 (iFGF23), (C) intact to total FGF23 ratio (i/c FGF23), (D) parathyroid hormone (PTH), (E) 1,25-dihydroxyvitamin D [1,25(OH)2D], (F) calcium (Ca2+), and (G) phosphate (Pi); (H) fractional excretion of Pi (FePi); and kidney mRNA expression of (I) NaPi2a, (J) Cyp27b1, and (K) Cyp24a1 in 12-week-old WT (n ≥ 5), Fgf23Dmp1-cKO (n ≥ 5), Dmp1KO (n ≥ 3), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 5) mice. Values are expressed as mean ± SEM; P < 0.05 vs. aWT,

Techniques: Expressing

Figure 3. Osteocyte-specific deletion of Fgf23 partially corrects bone growth in Dmp1KO mice. (A) Mouse gross appearance, (B) body weight, (C) tail length, (D) femur length, (E) femur gross appear- ance, and (F) 3D μCT representation of total femur in sagittal plane (scale bar = 1 mm) in 12-week- old WT (n ≥ 6), Fgf23Dmp1-cKO (n ≥ 5), Dmp1KO (n ≥ 5), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 4) mice. Values are expressed as mean ± SEM; P < 0.05 vs. aWT,

Journal: JCI insight

Article Title: FGF23 directly inhibits osteoprogenitor differentiation in Dmp1-knockout mice.

doi: 10.1172/jci.insight.156850

Figure Lengend Snippet: Figure 3. Osteocyte-specific deletion of Fgf23 partially corrects bone growth in Dmp1KO mice. (A) Mouse gross appearance, (B) body weight, (C) tail length, (D) femur length, (E) femur gross appear- ance, and (F) 3D μCT representation of total femur in sagittal plane (scale bar = 1 mm) in 12-week- old WT (n ≥ 6), Fgf23Dmp1-cKO (n ≥ 5), Dmp1KO (n ≥ 5), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 4) mice. Values are expressed as mean ± SEM; P < 0.05 vs. aWT,

Techniques:

Figure 4. Osteocyte-specific deletion of Fgf23 partially restores bone microarchitecture in Dmp1KO mice. 3D μCT (A) scan reconstruction of distal femur trabecular metaphysis (scale bar = 500 μm) and (B–G) parameters of trabecular bone microarchitecture; (H) scan reconstruction of midshaft femur cortical diaphysis (scale bar = 500 μm) and (I–O) parameters of cortical bone microarchitecture. All analyses were performed in 12-week-old WT (n ≥ 5), Fgf23Dmp1-cKO (n ≥ 5), Dmp1KO (n ≥ 5), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 5) mice. Values are expressed as mean ± SEM; P < 0.05 vs. aWT, bFgf23cKO, cDmp1KO. Statistical tests were ANOVA test followed by post hoc t tests and multiple-testing correction using Holm-Bonferroni method. BV/TV, bone volume to tissue volume ratio; Tb.N, trabecular number; Tb.Th, trabecular thickness; Tb.Sp, trabecular separation; Conn.Dens, connectivity density; SMI, structural model index; mat BMD, material bone mineral density; Ma.Ar, marrow area; CSA, cross-sectional area; Ct.Ar, cortical area; Ct.Th, cortical thickness; Ct.Po, cortical porosity.

Journal: JCI insight

Article Title: FGF23 directly inhibits osteoprogenitor differentiation in Dmp1-knockout mice.

doi: 10.1172/jci.insight.156850

Figure Lengend Snippet: Figure 4. Osteocyte-specific deletion of Fgf23 partially restores bone microarchitecture in Dmp1KO mice. 3D μCT (A) scan reconstruction of distal femur trabecular metaphysis (scale bar = 500 μm) and (B–G) parameters of trabecular bone microarchitecture; (H) scan reconstruction of midshaft femur cortical diaphysis (scale bar = 500 μm) and (I–O) parameters of cortical bone microarchitecture. All analyses were performed in 12-week-old WT (n ≥ 5), Fgf23Dmp1-cKO (n ≥ 5), Dmp1KO (n ≥ 5), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 5) mice. Values are expressed as mean ± SEM; P < 0.05 vs. aWT, bFgf23cKO, cDmp1KO. Statistical tests were ANOVA test followed by post hoc t tests and multiple-testing correction using Holm-Bonferroni method. BV/TV, bone volume to tissue volume ratio; Tb.N, trabecular number; Tb.Th, trabecular thickness; Tb.Sp, trabecular separation; Conn.Dens, connectivity density; SMI, structural model index; mat BMD, material bone mineral density; Ma.Ar, marrow area; CSA, cross-sectional area; Ct.Ar, cortical area; Ct.Th, cortical thickness; Ct.Po, cortical porosity.

Techniques:

Figure 5. Osteocyte-specific deletion of Fgf23 partially restores mineralization and lacuno-canalicular network in Dmp1KO mice. (A and B) High-resolu- tion μCT analysis of cortical bone porosity (scale bar = 100 μm), (C) acid-etched scanning electron microscopy of femur cortical bone (scale bar = 20 μm), (D) red fluorescence microscopy imaging of ARS-stained mineralization fronts (top), and bright-field microscopy imaging of modified trichrome Goldner staining (middle) and tartrate-resistant acidic phosphatase (TRAcP) staining (bottom) of longitudinal histology sections of distal femur (scale bar = 100 μm for ARS, 250 μm for Goldner and TRAcP). For each staining, top (×3.5 original magnification) and bottom (×1.8 original magnification) zoom-in panels represent regions of interest in trabecular and in cortical bone, respectively. All analyses were performed in 12-week-old WT (n ≥ 5), Fgf23Dmp1-cKO (n ≥ 5), Dmp1KO (n ≥ 5), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 5) mice.

Journal: JCI insight

Article Title: FGF23 directly inhibits osteoprogenitor differentiation in Dmp1-knockout mice.

doi: 10.1172/jci.insight.156850

Figure Lengend Snippet: Figure 5. Osteocyte-specific deletion of Fgf23 partially restores mineralization and lacuno-canalicular network in Dmp1KO mice. (A and B) High-resolu- tion μCT analysis of cortical bone porosity (scale bar = 100 μm), (C) acid-etched scanning electron microscopy of femur cortical bone (scale bar = 20 μm), (D) red fluorescence microscopy imaging of ARS-stained mineralization fronts (top), and bright-field microscopy imaging of modified trichrome Goldner staining (middle) and tartrate-resistant acidic phosphatase (TRAcP) staining (bottom) of longitudinal histology sections of distal femur (scale bar = 100 μm for ARS, 250 μm for Goldner and TRAcP). For each staining, top (×3.5 original magnification) and bottom (×1.8 original magnification) zoom-in panels represent regions of interest in trabecular and in cortical bone, respectively. All analyses were performed in 12-week-old WT (n ≥ 5), Fgf23Dmp1-cKO (n ≥ 5), Dmp1KO (n ≥ 5), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 5) mice.

Techniques: Electron Microscopy, Fluorescence, Microscopy, Imaging, Staining, Modification

Figure 6. Osteocyte-specific deletion of Fgf23 restores osteoblast differentiation but does not restore impaired mineralization in Dmp1KO primary osteoblast cultures. Bone marrow stromal cells were isolated from 12-week-old WT (n ≥ 3), Fgf23Dmp1-cKO (n ≥ 3), Dmp1KO (n ≥ 3), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 4) mice, then cultured for 14 (D14) and 21 (D21) days in osteoblast differentiation medium containing 3, 7, or 10 mM of beta-glycerophosphate (bGP). Levels of (A) total DMP1 (cDMP1) and (B) total FGF23 (cFGF23) in conditioned media collected at D21. (C and D) Alkaline phosphatase (ALP) staining and quantification and (E and F) alizarin red S (ARS) staining and quantification. Values are expressed as mean ± SEM; P < 0.05 vs. bGP treatment–matched

Journal: JCI insight

Article Title: FGF23 directly inhibits osteoprogenitor differentiation in Dmp1-knockout mice.

doi: 10.1172/jci.insight.156850

Figure Lengend Snippet: Figure 6. Osteocyte-specific deletion of Fgf23 restores osteoblast differentiation but does not restore impaired mineralization in Dmp1KO primary osteoblast cultures. Bone marrow stromal cells were isolated from 12-week-old WT (n ≥ 3), Fgf23Dmp1-cKO (n ≥ 3), Dmp1KO (n ≥ 3), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 4) mice, then cultured for 14 (D14) and 21 (D21) days in osteoblast differentiation medium containing 3, 7, or 10 mM of beta-glycerophosphate (bGP). Levels of (A) total DMP1 (cDMP1) and (B) total FGF23 (cFGF23) in conditioned media collected at D21. (C and D) Alkaline phosphatase (ALP) staining and quantification and (E and F) alizarin red S (ARS) staining and quantification. Values are expressed as mean ± SEM; P < 0.05 vs. bGP treatment–matched

Techniques: Isolation, Cell Culture, Staining

Figure 7. Canonical pathways altered in Dmp1KO osteoblasts are differentially regulated by FGF23 and by DMP1. Bulk RNA-sequencing analysis was performed on bone marrow stromal cells isolated from 12-week-old WT (n = 3), Fgf23Dmp1-cKO (n = 3), Dmp1KO (n = 3), and Dmp1KO Fgf23Dmp1-cKO (n = 3) mice and cultured for 21 days in osteoblast differentiation medium containing 10 mM of beta-glycerophosphate. (A) Venn diagram identifies genes showing altered expression in Dmp1KO but not in Dmp1KO Fgf23cKO osteoblasts (tan area). Heatmaps represent the expression of (B) Fgf23 and (C) genes identified in A and used in Ingenuity Pathway Analysis (IPA; QIAGEN) to define the most represented canonical pathways regulated by FGF23. (D) Venn diagram identifies genes showing altered expression in Dmp1KO and in Dmp1KO Fgf23cKO osteoblasts (burgundy area). Heatmaps represent the expression of (E) Dmp1 and (F) genes identified in D and used in IPA to define the most represented canonical pathways regulated by DMP1. Statistical tests were unpaired t test and corrected by the false discovery rate (P < 0.1).

Journal: JCI insight

Article Title: FGF23 directly inhibits osteoprogenitor differentiation in Dmp1-knockout mice.

doi: 10.1172/jci.insight.156850

Figure Lengend Snippet: Figure 7. Canonical pathways altered in Dmp1KO osteoblasts are differentially regulated by FGF23 and by DMP1. Bulk RNA-sequencing analysis was performed on bone marrow stromal cells isolated from 12-week-old WT (n = 3), Fgf23Dmp1-cKO (n = 3), Dmp1KO (n = 3), and Dmp1KO Fgf23Dmp1-cKO (n = 3) mice and cultured for 21 days in osteoblast differentiation medium containing 10 mM of beta-glycerophosphate. (A) Venn diagram identifies genes showing altered expression in Dmp1KO but not in Dmp1KO Fgf23cKO osteoblasts (tan area). Heatmaps represent the expression of (B) Fgf23 and (C) genes identified in A and used in Ingenuity Pathway Analysis (IPA; QIAGEN) to define the most represented canonical pathways regulated by FGF23. (D) Venn diagram identifies genes showing altered expression in Dmp1KO and in Dmp1KO Fgf23cKO osteoblasts (burgundy area). Heatmaps represent the expression of (E) Dmp1 and (F) genes identified in D and used in IPA to define the most represented canonical pathways regulated by DMP1. Statistical tests were unpaired t test and corrected by the false discovery rate (P < 0.1).

Techniques: RNA Sequencing, Isolation, Cell Culture, Expressing

Figure 9. FGF23 targets osteoprogenitors via FGFR/ERK/PI3K signaling. Single-cell RNA-sequencing analysis was performed on bone marrow stromal cells isolated from 12-week-old WT (n = 3), Fgf23Dmp1-cKO (n = 3), Dmp1KO (n = 3), and Dmp1KO Fgf23Dmp1-cKO (n = 3) mice and cultured for 21 days in osteoblast differentiation medium containing 10 mM of beta-glycerophosphate. (A) Venn diagram identifies genes showing altered expression in Dmp1KO but not in Dmp1KO Fgf23cKO osteoblasts (colored area) in each cluster of differentiation. (B) Heatmaps represent the expression of genes identified in A in the osteo- progenitor cluster (green dot) and used in Ingenuity Pathway Analysis (IPA) to define the most represented canonical pathways regulated by FGF23. (C–J) Violin plots representing the expression of most regulated target genes in Dmp1KO and corrected in Dmp1KO Fgf23cKO osteoprogenitors. (K) IPA gene network analysis showing most connected gene targets in the osteoprogenitor cluster and identifying FGF receptor 1 (FGFR1), ERK1/2, and PI3K/AKT as common regulators of these targets. Statistical tests were Mann-Whitney’s U test and corrected by the false discovery rate (P < 0.1).

Journal: JCI insight

Article Title: FGF23 directly inhibits osteoprogenitor differentiation in Dmp1-knockout mice.

doi: 10.1172/jci.insight.156850

Figure Lengend Snippet: Figure 9. FGF23 targets osteoprogenitors via FGFR/ERK/PI3K signaling. Single-cell RNA-sequencing analysis was performed on bone marrow stromal cells isolated from 12-week-old WT (n = 3), Fgf23Dmp1-cKO (n = 3), Dmp1KO (n = 3), and Dmp1KO Fgf23Dmp1-cKO (n = 3) mice and cultured for 21 days in osteoblast differentiation medium containing 10 mM of beta-glycerophosphate. (A) Venn diagram identifies genes showing altered expression in Dmp1KO but not in Dmp1KO Fgf23cKO osteoblasts (colored area) in each cluster of differentiation. (B) Heatmaps represent the expression of genes identified in A in the osteo- progenitor cluster (green dot) and used in Ingenuity Pathway Analysis (IPA) to define the most represented canonical pathways regulated by FGF23. (C–J) Violin plots representing the expression of most regulated target genes in Dmp1KO and corrected in Dmp1KO Fgf23cKO osteoprogenitors. (K) IPA gene network analysis showing most connected gene targets in the osteoprogenitor cluster and identifying FGF receptor 1 (FGFR1), ERK1/2, and PI3K/AKT as common regulators of these targets. Statistical tests were Mann-Whitney’s U test and corrected by the false discovery rate (P < 0.1).

Techniques: RNA Sequencing, Isolation, Cell Culture, Expressing

Figure 10. FGF23 directly inhibits osteoblast differentiation. (A–C) mRNA expression of markers of osteoblast differentiation in MC3T3-E1 osteoblasts cultured for 21 days and treated with recombinant FGF23 (0, 25, and 50 ng/mL) for the last 6 and 48 hours of culture (n ≥ 4). Levels of (D) total DMP1 (cDMP1) and (E) total FGF23 (cFGF23) measured by ELISA in conditioned culture media from bone marrow stromal cells (BMSCs) isolated from 12-week-old WT (n ≥ 4), Fgf23Dmp1-cKO (n ≥ 5), Dmp1KO (n ≥ 5), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 5) mice, then cocultured for 21 days with BMSCs iso- lated from the same group (isogenic), or immor- talized BMSCs displaying genetic overexpression of Fgf23 (Fgf23TG) or Dmp1 (Dmp1TG). (F and G) Alkaline phosphatase (ALP) staining and quanti- fication and (H and I) alizarin red S (ARS) staining and quantification. Values are expressed as mean ± SEM; P < 0.05 vs. (A–C) time point–matched

Journal: JCI insight

Article Title: FGF23 directly inhibits osteoprogenitor differentiation in Dmp1-knockout mice.

doi: 10.1172/jci.insight.156850

Figure Lengend Snippet: Figure 10. FGF23 directly inhibits osteoblast differentiation. (A–C) mRNA expression of markers of osteoblast differentiation in MC3T3-E1 osteoblasts cultured for 21 days and treated with recombinant FGF23 (0, 25, and 50 ng/mL) for the last 6 and 48 hours of culture (n ≥ 4). Levels of (D) total DMP1 (cDMP1) and (E) total FGF23 (cFGF23) measured by ELISA in conditioned culture media from bone marrow stromal cells (BMSCs) isolated from 12-week-old WT (n ≥ 4), Fgf23Dmp1-cKO (n ≥ 5), Dmp1KO (n ≥ 5), and Dmp1KO Fgf23Dmp1-cKO (n ≥ 5) mice, then cocultured for 21 days with BMSCs iso- lated from the same group (isogenic), or immor- talized BMSCs displaying genetic overexpression of Fgf23 (Fgf23TG) or Dmp1 (Dmp1TG). (F and G) Alkaline phosphatase (ALP) staining and quanti- fication and (H and I) alizarin red S (ARS) staining and quantification. Values are expressed as mean ± SEM; P < 0.05 vs. (A–C) time point–matched

Techniques: Expressing, Cell Culture, Recombinant, Enzyme-linked Immunosorbent Assay, Isolation, Over Expression, Staining

Figure 10. Transcriptional implications of treatments at Cyp27b1. ChIP-Seq analysis near Cyp27b1 for (A) BRD4, (B) RNA polymerase II, and (C) H3K36me3 from WT mice injected with 230 mg/kg bw PTH (30 min, PTH30), 30 mg/kg bw YKL-05 to 099 (1 h), 40 mg/kg bw SK-124 (1 h), 10 mg/kg bw 1,25(OH)2D3 (1 h), or 50 mg/kg bw FGF23 (1 h). Additional details as for Figure 2. Genomic region displayed is chr10: 126,469,260 to 126,490,800. bw, body weight; ChIP- Seq, chromatin immunoprecipitation; FGF23, ﬁbroblast growth factor 23; 1,25(OH)2D3, 1,25-dihydroxyvitamin D3; PTH, parathyroid hormone.

Journal: The Journal of biological chemistry

Article Title: Rapid genomic changes by mineralotropic hormones and kinase SIK inhibition drive coordinated renal Cyp27b1 and Cyp24a1 expression via CREB modules.

doi: 10.1016/j.jbc.2022.102559

Figure Lengend Snippet: Figure 10. Transcriptional implications of treatments at Cyp27b1. ChIP-Seq analysis near Cyp27b1 for (A) BRD4, (B) RNA polymerase II, and (C) H3K36me3 from WT mice injected with 230 mg/kg bw PTH (30 min, PTH30), 30 mg/kg bw YKL-05 to 099 (1 h), 40 mg/kg bw SK-124 (1 h), 10 mg/kg bw 1,25(OH)2D3 (1 h), or 50 mg/kg bw FGF23 (1 h). Additional details as for Figure 2. Genomic region displayed is chr10: 126,469,260 to 126,490,800. bw, body weight; ChIP- Seq, chromatin immunoprecipitation; FGF23, ﬁbroblast growth factor 23; 1,25(OH)2D3, 1,25-dihydroxyvitamin D3; PTH, parathyroid hormone.

Article Snippet: The following reagents were used for in vivo injections: 1α,25(OH)2D3 was obtained from SAFC Global, PTH (1–84 human) was obtained from Bachem (H-1370.0100), mouse FGF23 from R&D Systems (2629-FG-025), YKL-05-099 (27), and SK-124 (26).

Techniques: ChIP-sequencing, Injection, Chromatin Immunoprecipitation

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