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R&D Systems recombinant human fgf23
$Anti‐GBM disease causes tubular damage and partial renal resistance to <t>FGF23.</t> (A) Depicts the experimental workflow in male C57BL/6 mice undergoing induction of anti‐GBM disease using nephrotoxic serum followed by 6 days of intravenous (IV) FGF23 or vehicle treatment. (B) Shows the glomerular filtration rate of different experimental groups at days 0 and 7. (C) Shows urinary albumin/creatinine ratio at day 7. (D) Shows the example renal sections negative or positive for renal tubular casts (arrows) and quantitative tubular cast scores. (E) Shows plasma phosphate and fractional excretion of phosphate of healthy mice and mice with anti‐GBM treated with vehicle or FGF23. Analyses in panel (B): paired t ‐test. Analyses in panels (C–E): two‐way ANOVA. Anti‐GBM, anti‐glomerular basement membrane; d, disease state; t, treatment.$
Recombinant Human Fgf23, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+fgf23+protein/pmc12929185-42-0-6?v=R%26D+Systems
Average 94 stars, based on 40 article reviews

recombinant human fgf23 - by Bioz Stars, 2026-08

94/100 stars

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1) Product Images from "The renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease"

Article Title: The renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease

Journal: Journal of Cell Communication and Signaling

doi: 10.1002/ccs3.70061

$Anti‐GBM disease causes tubular damage and partial renal resistance to FGF23. (A) Depicts the experimental workflow in male C57BL/6 mice undergoing induction of anti‐GBM disease using nephrotoxic serum followed by 6 days of intravenous (IV) FGF23 or vehicle treatment. (B) Shows the glomerular filtration rate of different experimental groups at days 0 and 7. (C) Shows urinary albumin/creatinine ratio at day 7. (D) Shows the example renal sections negative or positive for renal tubular casts (arrows) and quantitative tubular cast scores. (E) Shows plasma phosphate and fractional excretion of phosphate of healthy mice and mice with anti‐GBM treated with vehicle or FGF23. Analyses in panel (B): paired t ‐test. Analyses in panels (C–E): two‐way ANOVA. Anti‐GBM, anti‐glomerular basement membrane; d, disease state; t, treatment.$
Figure Legend Snippet: Anti‐GBM disease causes tubular damage and partial renal resistance to FGF23. (A) Depicts the experimental workflow in male C57BL/6 mice undergoing induction of anti‐GBM disease using nephrotoxic serum followed by 6 days of intravenous (IV) FGF23 or vehicle treatment. (B) Shows the glomerular filtration rate of different experimental groups at days 0 and 7. (C) Shows urinary albumin/creatinine ratio at day 7. (D) Shows the example renal sections negative or positive for renal tubular casts (arrows) and quantitative tubular cast scores. (E) Shows plasma phosphate and fractional excretion of phosphate of healthy mice and mice with anti‐GBM treated with vehicle or FGF23. Analyses in panel (B): paired t ‐test. Analyses in panels (C–E): two‐way ANOVA. Anti‐GBM, anti‐glomerular basement membrane; d, disease state; t, treatment.

Techniques Used: Filtration, Clinical Proteomics, Membrane

Six‐day course of FGF23 treatment induces renal transcriptional signatures of inflammatory responses and injury. (A) Indicates the number of differentially expressed genes according to experimental comparison in renal bulk RNA‐Seq. (B, C) Depict volcano plots of DEGs above a cutoff of adjusted p < 0.05 and log2‐fold change >1, in the comparison of FGF23 versus vehicle effect in mice with anti‐GBM (B) and the interaction between treatment and disease effect (C). (D–F) Depict significant Reactome gene set enrichment analyses of FGF23 effects in healthy mice (D), mice with anti‐GBM disease (E), and the interaction between treatment and disease effect (F). (G) Depicts a network of ligand–receptor interaction pairs that were significant for FGF23 versus vehicle comparisons in mice with anti‐GBM disease by bulk RNA‐Seq. The ligand–receptor interactions were inferred using R/BulkSignalR. Anti‐GBM, anti‐glomerular basement membrane disease. N = 3 for anti‐GBM groups and n = 4 for healthy groups.

Figure Legend Snippet: Six‐day course of FGF23 treatment induces renal transcriptional signatures of inflammatory responses and injury. (A) Indicates the number of differentially expressed genes according to experimental comparison in renal bulk RNA‐Seq. (B, C) Depict volcano plots of DEGs above a cutoff of adjusted p < 0.05 and log2‐fold change >1, in the comparison of FGF23 versus vehicle effect in mice with anti‐GBM (B) and the interaction between treatment and disease effect (C). (D–F) Depict significant Reactome gene set enrichment analyses of FGF23 effects in healthy mice (D), mice with anti‐GBM disease (E), and the interaction between treatment and disease effect (F). (G) Depicts a network of ligand–receptor interaction pairs that were significant for FGF23 versus vehicle comparisons in mice with anti‐GBM disease by bulk RNA‐Seq. The ligand–receptor interactions were inferred using R/BulkSignalR. Anti‐GBM, anti‐glomerular basement membrane disease. N = 3 for anti‐GBM groups and n = 4 for healthy groups.

Techniques Used: Comparison, RNA Sequencing, Membrane

Bulk RNA‐Seq deconvolution and immunofluorescence staining reveal an FGF23‐driven increase in overall immune cell and macrophage abundance in the kidneys of mice with anti‐GBM disease. (A, B) Depict the annotation of renal cell clusters in the reanalysis of the single‐cell RNA‐Seq dataset GSE107585 of murine kidney from 7 sex‐mixed healthy C57BL/6 mice; see also Supporting Information Figure . (C) Shows a wedding pie plot of the bulk deconvolution of the renal cellular composition according to FGF23 treatment and anti‐GBM disease state, as indicated by labels. Overall renal immune cells and macrophage‐like cells are displayed by bulk deconvolution (D, G) and by immunofluorescence with automated quantification for CD45 (E, F) and F4/80 (H, I). RNA‐Seq: N = 3 for anti‐GBM groups and n = 4 for healthy groups. Immunofluorescence: n = 4 per group. Statistical analysis: two‐way ANOVA. anti‐GBM, anti‐glomerular basement membrane disease; Baso, basophil; CD, collecting duct; d, disease state; DCT, distal convoluted tubule; DLOH, descending limb of Henle; EC, endothelial cell; Granul, granulocyte; i, interaction; IC, intercalated cells; Ly, lymphocyte; Mono, monocyte; Mph, macrophage; NK, natural killer cell; PC, principal cells; PT, proximal tubule; S, segment; t, treatment.

Figure Legend Snippet: Bulk RNA‐Seq deconvolution and immunofluorescence staining reveal an FGF23‐driven increase in overall immune cell and macrophage abundance in the kidneys of mice with anti‐GBM disease. (A, B) Depict the annotation of renal cell clusters in the reanalysis of the single‐cell RNA‐Seq dataset GSE107585 of murine kidney from 7 sex‐mixed healthy C57BL/6 mice; see also Supporting Information Figure . (C) Shows a wedding pie plot of the bulk deconvolution of the renal cellular composition according to FGF23 treatment and anti‐GBM disease state, as indicated by labels. Overall renal immune cells and macrophage‐like cells are displayed by bulk deconvolution (D, G) and by immunofluorescence with automated quantification for CD45 (E, F) and F4/80 (H, I). RNA‐Seq: N = 3 for anti‐GBM groups and n = 4 for healthy groups. Immunofluorescence: n = 4 per group. Statistical analysis: two‐way ANOVA. anti‐GBM, anti‐glomerular basement membrane disease; Baso, basophil; CD, collecting duct; d, disease state; DCT, distal convoluted tubule; DLOH, descending limb of Henle; EC, endothelial cell; Granul, granulocyte; i, interaction; IC, intercalated cells; Ly, lymphocyte; Mono, monocyte; Mph, macrophage; NK, natural killer cell; PC, principal cells; PT, proximal tubule; S, segment; t, treatment.

Techniques Used: RNA Sequencing, Immunofluorescence, Staining, Single Cell, Membrane

Immune protein profiling highlights an increase in circulating soluble tumor necrosis factor receptors induced by FGF23 and anti‐GBM disease in mice. A plasma cytokine protein array shows FGF23 effects in healthy male C57BL/6 mice (A) and in mice treated with nephrotoxic serum to induce anti‐GBM disease (B). The interaction between treatment and disease state (C) and the overall disease effect (D) are shown. (E–F) Depict analyses of soluble TNF receptors 1 and 2 by two‐way ANOVA. d, disease state; t, treatment. N = 4 biologically independent replicates per group. Anti‐GBM, anti‐glomerular basement membrane.

Figure Legend Snippet: Immune protein profiling highlights an increase in circulating soluble tumor necrosis factor receptors induced by FGF23 and anti‐GBM disease in mice. A plasma cytokine protein array shows FGF23 effects in healthy male C57BL/6 mice (A) and in mice treated with nephrotoxic serum to induce anti‐GBM disease (B). The interaction between treatment and disease state (C) and the overall disease effect (D) are shown. (E–F) Depict analyses of soluble TNF receptors 1 and 2 by two‐way ANOVA. d, disease state; t, treatment. N = 4 biologically independent replicates per group. Anti‐GBM, anti‐glomerular basement membrane.

Techniques Used: Clinical Proteomics, Protein Array, Membrane

$Renal immune cell recruitment driven by FGF23 excess is exposure time dependent. Renal microarray transcriptome datasets GDS3361 of male Fgf23 transgenic and control mice or sex‐matched Hyp mice of dataset GDS879 (B) underwent bulk deconvolution with reference to single‐cell RNA‐Seq dataset GSE107585 of murine kidney from 7 sex‐mixed healthy C57BL/6 mice and, subsequently, visualization of overall fractions of inferred immune cells and macrophage‐like cells, as indicated. (C) Shows the experimental workflow of experiments with female BALB/c mice undergoing Adriamycin (doxorubicin) nephropathy followed by a single intravenous (IV) injection of FGF23 or vehicle. (D) Shows the urinary albumin/creatinine ratio 7 days after induction of Adriamycin nephropathy. Statistical analysis: two‐way ANOVA. d, disease state. (E–G) Show significant Reactome gene set enrichment analyses of renal FGF23 effects in healthy mice (E), mice with Adriamycin nephropathy (F), and the interaction between treatment and disease effect (G). (H) Depicts the log‐fold change of 8 transcripts with lowest adjusted p ‐value in the interaction analysis of FGF23 effect in diseased versus FGF23 effect in healthy mice in a 2 × 2 factorial design. N = 5 (A), 10 (B), or 4 (C–H) biologically independent replicates per group.$
Figure Legend Snippet: Renal immune cell recruitment driven by FGF23 excess is exposure time dependent. Renal microarray transcriptome datasets GDS3361 of male Fgf23 transgenic and control mice or sex‐matched Hyp mice of dataset GDS879 (B) underwent bulk deconvolution with reference to single‐cell RNA‐Seq dataset GSE107585 of murine kidney from 7 sex‐mixed healthy C57BL/6 mice and, subsequently, visualization of overall fractions of inferred immune cells and macrophage‐like cells, as indicated. (C) Shows the experimental workflow of experiments with female BALB/c mice undergoing Adriamycin (doxorubicin) nephropathy followed by a single intravenous (IV) injection of FGF23 or vehicle. (D) Shows the urinary albumin/creatinine ratio 7 days after induction of Adriamycin nephropathy. Statistical analysis: two‐way ANOVA. d, disease state. (E–G) Show significant Reactome gene set enrichment analyses of renal FGF23 effects in healthy mice (E), mice with Adriamycin nephropathy (F), and the interaction between treatment and disease effect (G). (H) Depicts the log‐fold change of 8 transcripts with lowest adjusted p ‐value in the interaction analysis of FGF23 effect in diseased versus FGF23 effect in healthy mice in a 2 × 2 factorial design. N = 5 (A), 10 (B), or 4 (C–H) biologically independent replicates per group.

Techniques Used: Microarray, Transgenic Assay, Control, Single Cell, RNA Sequencing, IV Injection

Intrarenal proinflammatory effects of FGF23 applied ex vivo in PCKS. (A) Male DBA/2J mice underwent dietary treatment with 0.2% adenine for 15 weeks, followed by organ collection and preparation of 300 µm PCKS for a 24‐h treatment with FGF23 or vehicle ex vivo. No disease‐free controls were used for this substudy. (B) Depicts the fibrotic changes in a representative 4 µm section of PCKS stained with hematoxylin and eosin (left scale bar, 500 µm; right, 100 µm). (C) Shows the log‐fold change of upregulated transcripts with the lowest adjusted p ‐value in the FGF23 versus vehicle comparison. (D–F) Show gene set enrichment analyses of FGF23 effects in Reactome (D), WikiPathways (E), and Pathway Interaction Database (F) gene sets. N = 4 biologically independent replicates per group. PCKS, precision‐cut kidney slices.

Figure Legend Snippet: Intrarenal proinflammatory effects of FGF23 applied ex vivo in PCKS. (A) Male DBA/2J mice underwent dietary treatment with 0.2% adenine for 15 weeks, followed by organ collection and preparation of 300 µm PCKS for a 24‐h treatment with FGF23 or vehicle ex vivo. No disease‐free controls were used for this substudy. (B) Depicts the fibrotic changes in a representative 4 µm section of PCKS stained with hematoxylin and eosin (left scale bar, 500 µm; right, 100 µm). (C) Shows the log‐fold change of upregulated transcripts with the lowest adjusted p ‐value in the FGF23 versus vehicle comparison. (D–F) Show gene set enrichment analyses of FGF23 effects in Reactome (D), WikiPathways (E), and Pathway Interaction Database (F) gene sets. N = 4 biologically independent replicates per group. PCKS, precision‐cut kidney slices.

Techniques Used: Ex Vivo, Staining, Comparison

FGF23 is associated with renal immune cell content in human patients with IgA nephropathy. As a reference, single‐nucleus RNA‐Seq data from 5 human kidney biopsies ( GSE199711 ) of 2 healthy controls and 3 patients with chronic kidney disease (CKD) were reanalyzed and annotated (A); see also Supporting Information Figure . 35 patients with IgA nephropathy from the Karolinska Kidney Biopsy Cohort showed an inverse univariable association between circulating FGF23 and measured glomerular filtration rate (GFR) (B). The associations between transcriptome‐inferred renal fibroblasts and immune cells (C–D) or macrophages (E–F) and circulating FGF23 are shown, with adjustment for GFR, 25OH‐vitamin D and parathyroid hormone. (D, F) Show disaggregated data stratified by GFR in CKD stages I–II and III–V.

Figure Legend Snippet: FGF23 is associated with renal immune cell content in human patients with IgA nephropathy. As a reference, single‐nucleus RNA‐Seq data from 5 human kidney biopsies ( GSE199711 ) of 2 healthy controls and 3 patients with chronic kidney disease (CKD) were reanalyzed and annotated (A); see also Supporting Information Figure . 35 patients with IgA nephropathy from the Karolinska Kidney Biopsy Cohort showed an inverse univariable association between circulating FGF23 and measured glomerular filtration rate (GFR) (B). The associations between transcriptome‐inferred renal fibroblasts and immune cells (C–D) or macrophages (E–F) and circulating FGF23 are shown, with adjustment for GFR, 25OH‐vitamin D and parathyroid hormone. (D, F) Show disaggregated data stratified by GFR in CKD stages I–II and III–V.

Techniques Used: RNA Sequencing, Filtration

Image Search Results

Journal: Journal of Cell Communication and Signaling

Article Title: The renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease

doi: 10.1002/ccs3.70061

Figure Lengend Snippet: Anti‐GBM disease causes tubular damage and partial renal resistance to FGF23. (A) Depicts the experimental workflow in male C57BL/6 mice undergoing induction of anti‐GBM disease using nephrotoxic serum followed by 6 days of intravenous (IV) FGF23 or vehicle treatment. (B) Shows the glomerular filtration rate of different experimental groups at days 0 and 7. (C) Shows urinary albumin/creatinine ratio at day 7. (D) Shows the example renal sections negative or positive for renal tubular casts (arrows) and quantitative tubular cast scores. (E) Shows plasma phosphate and fractional excretion of phosphate of healthy mice and mice with anti‐GBM treated with vehicle or FGF23. Analyses in panel (B): paired t ‐test. Analyses in panels (C–E): two‐way ANOVA. Anti‐GBM, anti‐glomerular basement membrane; d, disease state; t, treatment.

Article Snippet: Recombinant human FGF23 was obtained from R&D Systems, Minneapolis, MN, USA, and distributed via Thermo Fisher (Cat. #100‐52).

Techniques: Filtration, Clinical Proteomics, Membrane

Journal: Journal of Cell Communication and Signaling

Article Title: The renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease

doi: 10.1002/ccs3.70061

Figure Lengend Snippet: Six‐day course of FGF23 treatment induces renal transcriptional signatures of inflammatory responses and injury. (A) Indicates the number of differentially expressed genes according to experimental comparison in renal bulk RNA‐Seq. (B, C) Depict volcano plots of DEGs above a cutoff of adjusted p < 0.05 and log2‐fold change >1, in the comparison of FGF23 versus vehicle effect in mice with anti‐GBM (B) and the interaction between treatment and disease effect (C). (D–F) Depict significant Reactome gene set enrichment analyses of FGF23 effects in healthy mice (D), mice with anti‐GBM disease (E), and the interaction between treatment and disease effect (F). (G) Depicts a network of ligand–receptor interaction pairs that were significant for FGF23 versus vehicle comparisons in mice with anti‐GBM disease by bulk RNA‐Seq. The ligand–receptor interactions were inferred using R/BulkSignalR. Anti‐GBM, anti‐glomerular basement membrane disease. N = 3 for anti‐GBM groups and n = 4 for healthy groups.

Article Snippet: Recombinant human FGF23 was obtained from R&D Systems, Minneapolis, MN, USA, and distributed via Thermo Fisher (Cat. #100‐52).

Techniques: Comparison, RNA Sequencing, Membrane

Journal: Journal of Cell Communication and Signaling

Article Title: The renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease

doi: 10.1002/ccs3.70061

Figure Lengend Snippet: Bulk RNA‐Seq deconvolution and immunofluorescence staining reveal an FGF23‐driven increase in overall immune cell and macrophage abundance in the kidneys of mice with anti‐GBM disease. (A, B) Depict the annotation of renal cell clusters in the reanalysis of the single‐cell RNA‐Seq dataset GSE107585 of murine kidney from 7 sex‐mixed healthy C57BL/6 mice; see also Supporting Information Figure . (C) Shows a wedding pie plot of the bulk deconvolution of the renal cellular composition according to FGF23 treatment and anti‐GBM disease state, as indicated by labels. Overall renal immune cells and macrophage‐like cells are displayed by bulk deconvolution (D, G) and by immunofluorescence with automated quantification for CD45 (E, F) and F4/80 (H, I). RNA‐Seq: N = 3 for anti‐GBM groups and n = 4 for healthy groups. Immunofluorescence: n = 4 per group. Statistical analysis: two‐way ANOVA. anti‐GBM, anti‐glomerular basement membrane disease; Baso, basophil; CD, collecting duct; d, disease state; DCT, distal convoluted tubule; DLOH, descending limb of Henle; EC, endothelial cell; Granul, granulocyte; i, interaction; IC, intercalated cells; Ly, lymphocyte; Mono, monocyte; Mph, macrophage; NK, natural killer cell; PC, principal cells; PT, proximal tubule; S, segment; t, treatment.

Article Snippet: Recombinant human FGF23 was obtained from R&D Systems, Minneapolis, MN, USA, and distributed via Thermo Fisher (Cat. #100‐52).

Techniques: RNA Sequencing, Immunofluorescence, Staining, Single Cell, Membrane

Journal: Journal of Cell Communication and Signaling

Article Title: The renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease

doi: 10.1002/ccs3.70061

Figure Lengend Snippet: Immune protein profiling highlights an increase in circulating soluble tumor necrosis factor receptors induced by FGF23 and anti‐GBM disease in mice. A plasma cytokine protein array shows FGF23 effects in healthy male C57BL/6 mice (A) and in mice treated with nephrotoxic serum to induce anti‐GBM disease (B). The interaction between treatment and disease state (C) and the overall disease effect (D) are shown. (E–F) Depict analyses of soluble TNF receptors 1 and 2 by two‐way ANOVA. d, disease state; t, treatment. N = 4 biologically independent replicates per group. Anti‐GBM, anti‐glomerular basement membrane.

Article Snippet: Recombinant human FGF23 was obtained from R&D Systems, Minneapolis, MN, USA, and distributed via Thermo Fisher (Cat. #100‐52).

Techniques: Clinical Proteomics, Protein Array, Membrane

Journal: Journal of Cell Communication and Signaling

Article Title: The renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease

doi: 10.1002/ccs3.70061

Figure Lengend Snippet: Renal immune cell recruitment driven by FGF23 excess is exposure time dependent. Renal microarray transcriptome datasets GDS3361 of male Fgf23 transgenic and control mice or sex‐matched Hyp mice of dataset GDS879 (B) underwent bulk deconvolution with reference to single‐cell RNA‐Seq dataset GSE107585 of murine kidney from 7 sex‐mixed healthy C57BL/6 mice and, subsequently, visualization of overall fractions of inferred immune cells and macrophage‐like cells, as indicated. (C) Shows the experimental workflow of experiments with female BALB/c mice undergoing Adriamycin (doxorubicin) nephropathy followed by a single intravenous (IV) injection of FGF23 or vehicle. (D) Shows the urinary albumin/creatinine ratio 7 days after induction of Adriamycin nephropathy. Statistical analysis: two‐way ANOVA. d, disease state. (E–G) Show significant Reactome gene set enrichment analyses of renal FGF23 effects in healthy mice (E), mice with Adriamycin nephropathy (F), and the interaction between treatment and disease effect (G). (H) Depicts the log‐fold change of 8 transcripts with lowest adjusted p ‐value in the interaction analysis of FGF23 effect in diseased versus FGF23 effect in healthy mice in a 2 × 2 factorial design. N = 5 (A), 10 (B), or 4 (C–H) biologically independent replicates per group.

Article Snippet: Recombinant human FGF23 was obtained from R&D Systems, Minneapolis, MN, USA, and distributed via Thermo Fisher (Cat. #100‐52).

Techniques: Microarray, Transgenic Assay, Control, Single Cell, RNA Sequencing, IV Injection

Journal: Journal of Cell Communication and Signaling

Article Title: The renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease

doi: 10.1002/ccs3.70061

Figure Lengend Snippet: Intrarenal proinflammatory effects of FGF23 applied ex vivo in PCKS. (A) Male DBA/2J mice underwent dietary treatment with 0.2% adenine for 15 weeks, followed by organ collection and preparation of 300 µm PCKS for a 24‐h treatment with FGF23 or vehicle ex vivo. No disease‐free controls were used for this substudy. (B) Depicts the fibrotic changes in a representative 4 µm section of PCKS stained with hematoxylin and eosin (left scale bar, 500 µm; right, 100 µm). (C) Shows the log‐fold change of upregulated transcripts with the lowest adjusted p ‐value in the FGF23 versus vehicle comparison. (D–F) Show gene set enrichment analyses of FGF23 effects in Reactome (D), WikiPathways (E), and Pathway Interaction Database (F) gene sets. N = 4 biologically independent replicates per group. PCKS, precision‐cut kidney slices.

Article Snippet: Recombinant human FGF23 was obtained from R&D Systems, Minneapolis, MN, USA, and distributed via Thermo Fisher (Cat. #100‐52).

Techniques: Ex Vivo, Staining, Comparison

Journal: Journal of Cell Communication and Signaling

Article Title: The renal response to FGF23 shifts from phosphaturia toward inflammation in kidney disease

doi: 10.1002/ccs3.70061

Figure Lengend Snippet: FGF23 is associated with renal immune cell content in human patients with IgA nephropathy. As a reference, single‐nucleus RNA‐Seq data from 5 human kidney biopsies ( GSE199711 ) of 2 healthy controls and 3 patients with chronic kidney disease (CKD) were reanalyzed and annotated (A); see also Supporting Information Figure . 35 patients with IgA nephropathy from the Karolinska Kidney Biopsy Cohort showed an inverse univariable association between circulating FGF23 and measured glomerular filtration rate (GFR) (B). The associations between transcriptome‐inferred renal fibroblasts and immune cells (C–D) or macrophages (E–F) and circulating FGF23 are shown, with adjustment for GFR, 25OH‐vitamin D and parathyroid hormone. (D, F) Show disaggregated data stratified by GFR in CKD stages I–II and III–V.

Article Snippet: Recombinant human FGF23 was obtained from R&D Systems, Minneapolis, MN, USA, and distributed via Thermo Fisher (Cat. #100‐52).

Techniques: RNA Sequencing, Filtration

( 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 .

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

( 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 .

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

RGS14 truncation mutants were generated to identify functional domains suppressing hormone-regulated phosphate transport. ( A ) Serial deletions from the N-terminus of RGS14 were generated, as outlined in Experimental procedures. Previously characterized functional domains are depicted in the full-length (WT) RGS14 and the truncation mutants (1- – 4). Regulator of G protein Signaling (RGS) domain, Ras-binding domains 1 and 2 ( R1, R2 ), G protein regulatory (Go-Loco) motif, and -DSAL PDZ ligand are depicted. ( B ) Transfected WT-RGS14 and truncation mutants (constructs 1–4) expressed in HEK293 cells. Molecular weight markers (kDa) are presented for reference. Empty vector-transfected cell lysate (V) served as a negative control. ( C ) Hormone-sensitive phosphate uptake was measured in OK cells transfected with WT-RGS14 or the indicated truncation mutant. Phosphate transport was normalized to baseline phosphate uptake under control conditions (100%). Where indicated, cells were treated with 100 nM FGF23 or PTH before phosphate uptake measurements. n = 6. **** P < 0.001 vs . control.

Journal: Biochemical Journal

Article Title: Noncanonical RGS14 structural determinants control hormone-sensitive NPT2A-mediated phosphate transport

doi: 10.1042/BCJ20240122

Figure Lengend Snippet: RGS14 truncation mutants were generated to identify functional domains suppressing hormone-regulated phosphate transport. ( A ) Serial deletions from the N-terminus of RGS14 were generated, as outlined in Experimental procedures. Previously characterized functional domains are depicted in the full-length (WT) RGS14 and the truncation mutants (1- – 4). Regulator of G protein Signaling (RGS) domain, Ras-binding domains 1 and 2 ( R1, R2 ), G protein regulatory (Go-Loco) motif, and -DSAL PDZ ligand are depicted. ( B ) Transfected WT-RGS14 and truncation mutants (constructs 1–4) expressed in HEK293 cells. Molecular weight markers (kDa) are presented for reference. Empty vector-transfected cell lysate (V) served as a negative control. ( C ) Hormone-sensitive phosphate uptake was measured in OK cells transfected with WT-RGS14 or the indicated truncation mutant. Phosphate transport was normalized to baseline phosphate uptake under control conditions (100%). Where indicated, cells were treated with 100 nM FGF23 or PTH before phosphate uptake measurements. n = 6. **** P < 0.001 vs . control.

Article Snippet: Recombinant human Arg 179 Gln-FGF23 25-251 (herein referred to as FGF23), which is resistant to furin cleavage and inactivation, was obtained from R&D Systems (2604-FG-025).

Techniques: Generated, Functional Assay, Binding Assay, Transfection, Construct, Molecular Weight, Plasmid Preparation, Negative Control, Mutagenesis, Control

As indicated, OK cells were seeded on 12-well plates and transfected with RGS14 (WT or mutants) or empty vector (-). Cells were treated with 100 nM FGF23 or PTH for 2 hr, and Pi uptake was measured as detailed in Experimental procedures. Data were normalized to vector control (100%). ** P < 0.01 vs . control, *** P < 0.001 vs . control, **** P < 0.0001 vs control. n = 4.

Journal: Biochemical Journal

Article Title: Noncanonical RGS14 structural determinants control hormone-sensitive NPT2A-mediated phosphate transport

doi: 10.1042/BCJ20240122

Figure Lengend Snippet: As indicated, OK cells were seeded on 12-well plates and transfected with RGS14 (WT or mutants) or empty vector (-). Cells were treated with 100 nM FGF23 or PTH for 2 hr, and Pi uptake was measured as detailed in Experimental procedures. Data were normalized to vector control (100%). ** P < 0.01 vs . control, *** P < 0.001 vs . control, **** P < 0.0001 vs control. n = 4.

Article Snippet: Recombinant human Arg 179 Gln-FGF23 25-251 (herein referred to as FGF23), which is resistant to furin cleavage and inactivation, was obtained from R&D Systems (2604-FG-025).

Techniques: Transfection, Plasmid Preparation, Control

( A ) RGS14 Ser 266 Ala and Ser 269 Ala phosphorylation. HPCT cells expressing the indicated HA-RGS14 linker were treated with 100 nM PTH or FGF23 for 30 min or vehicle control ( C ). Cell lysates were prepared, and the linker peptide was immunoprecipitated with anti-HA agarose (Methods). The phosphorylated linker was assessed with an anti-phosphoserine antibody. Cell lysates exhibited comparable probe expression. Molecular weight markers (kDa) are shown on the right. Illustrative of n = 4. ( B ) Paired analysis of PTH and FGF23 effects on phosphorylation of the wild-typeWT linker peptide or the mutated Ser 266,269 Ala probe. ** P < 0.01. ( C ) Hormone-induced phosphorylation of full-length RGS14. HK-2 cells were transfected with FLAG-RGS14 and HA-NHERF1. After 24 h, cells were serum-starved overnight and then treated with 100 nM FGF23 or PTH for 30 min. FLAG-RGS14 was immunoprecipitated as detailed in Experimentalexperimental Proceduresprocedures. Molecular weight markers are shown to the right. Representative of n = 6. ( D ) Quantification of hormone-stimulated phosphorylation of full-length RGS14. ** P < 0.01. ( E ) PTH and FGF23 failed to promote phosphorylation in HK-2 cells transfected with FLAG-RGS14 but not HA-NHERF1.

Journal: Biochemical Journal

Article Title: Noncanonical RGS14 structural determinants control hormone-sensitive NPT2A-mediated phosphate transport

doi: 10.1042/BCJ20240122

Figure Lengend Snippet: ( A ) RGS14 Ser 266 Ala and Ser 269 Ala phosphorylation. HPCT cells expressing the indicated HA-RGS14 linker were treated with 100 nM PTH or FGF23 for 30 min or vehicle control ( C ). Cell lysates were prepared, and the linker peptide was immunoprecipitated with anti-HA agarose (Methods). The phosphorylated linker was assessed with an anti-phosphoserine antibody. Cell lysates exhibited comparable probe expression. Molecular weight markers (kDa) are shown on the right. Illustrative of n = 4. ( B ) Paired analysis of PTH and FGF23 effects on phosphorylation of the wild-typeWT linker peptide or the mutated Ser 266,269 Ala probe. ** P < 0.01. ( C ) Hormone-induced phosphorylation of full-length RGS14. HK-2 cells were transfected with FLAG-RGS14 and HA-NHERF1. After 24 h, cells were serum-starved overnight and then treated with 100 nM FGF23 or PTH for 30 min. FLAG-RGS14 was immunoprecipitated as detailed in Experimentalexperimental Proceduresprocedures. Molecular weight markers are shown to the right. Representative of n = 6. ( D ) Quantification of hormone-stimulated phosphorylation of full-length RGS14. ** P < 0.01. ( E ) PTH and FGF23 failed to promote phosphorylation in HK-2 cells transfected with FLAG-RGS14 but not HA-NHERF1.

Article Snippet: Recombinant human Arg 179 Gln-FGF23 25-251 (herein referred to as FGF23), which is resistant to furin cleavage and inactivation, was obtained from R&D Systems (2604-FG-025).

Techniques: Phospho-proteomics, Expressing, Control, Immunoprecipitation, Molecular Weight, Transfection

Working model of the role of RGS14 in controlling NPT2A-mediated phosphate uptake under resting conditions ( A ) and following stimulation with PTH or FGF23 ( B ). ( A ) NPT2A binds NHERF1 PDZ1 and human RGS14 binds PDZ2, stabilizing the [NHERF1:NPT2A] complex at the membrane surface permitting constitutive phosphate uptake. ( B ) PTH, acting through the PTH receptor (PTHR) or FGF23 through FGFR1, promotes RGS14 phosphorylation and its dissociation from NHERF1 leading to sequestration of NPT2A and cessation of phosphate uptake [ , ].

Journal: Biochemical Journal

Article Title: Noncanonical RGS14 structural determinants control hormone-sensitive NPT2A-mediated phosphate transport

doi: 10.1042/BCJ20240122

Figure Lengend Snippet: Working model of the role of RGS14 in controlling NPT2A-mediated phosphate uptake under resting conditions ( A ) and following stimulation with PTH or FGF23 ( B ). ( A ) NPT2A binds NHERF1 PDZ1 and human RGS14 binds PDZ2, stabilizing the [NHERF1:NPT2A] complex at the membrane surface permitting constitutive phosphate uptake. ( B ) PTH, acting through the PTH receptor (PTHR) or FGF23 through FGFR1, promotes RGS14 phosphorylation and its dissociation from NHERF1 leading to sequestration of NPT2A and cessation of phosphate uptake [ , ].

Article Snippet: Recombinant human Arg 179 Gln-FGF23 25-251 (herein referred to as FGF23), which is resistant to furin cleavage and inactivation, was obtained from R&D Systems (2604-FG-025).

Techniques: Membrane, Phospho-proteomics

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