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Charles River Laboratories ifgf23 levels
High phosphate, not the increase of fibroblast growth factor 23 (FGF23), drives tubular injury and perivascular tertiary lymphoid structure (TLS) formation. (a) Schematic representation of the study design including specific time points for adeno‐associated virus (AAV) treatment inducing the overexpression of fibroblast growth factor 23 (FGF23), dietary intervention, as well as biosampling and tissue collection. (b) Quantification of plasma <t>intact</t> <t>FGF23</t> <t>(iFGF23)</t> concentrations, serum phosphate (Pi), serum creatinine (Crea), and urinary albumin to creatinine ratio (ACR) in all three groups. (c) Representative images of the cortex of hematoxylin and eosin (HE), periodic acid‐Schiff (PAS), and picrosirius red stained kidney cross‐sections, as well as immunofluorescence (IF) staining of kidney injury molecule 1 (Kim‐1; orange) positive tubules. (d) Quantification of the scoring of tubular injury, of real‐time PCR analysis of Havcr1 , and of kidney fibrosis in the cortex. (e) Representative HE, PAS and picrosirius red staining focusing on the perivascular region of TLS development. (f) Representative IF costaining of CD45R + (green) and CD3 + (orange) lymphocytes, of CD45R (green) and Ki67 (orange), and of IgD (red) synthesis. (g) Quantification of lymphocytes using flow cytometry analysis of whole kidney tissue from mice of all three groups. (c, f) Counterstaining of cell nuclei using DAPI (blue). (c, e and f) Scale bars: 100 μm. (b, d, g) Data are presented as mean ± SD. One‐way analysis of variance (ANOVA) with Tukey's multiple comparisons test, * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. A, artery.
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1) Product Images from "High Phosphate Load Induces De Novo Formation of Tertiary Lymphoid Structures in the Kidney"

Article Title: High Phosphate Load Induces De Novo Formation of Tertiary Lymphoid Structures in the Kidney

Journal: The FASEB Journal

doi: 10.1096/fj.202500968R

High phosphate, not the increase of fibroblast growth factor 23 (FGF23), drives tubular injury and perivascular tertiary lymphoid structure (TLS) formation. (a) Schematic representation of the study design including specific time points for adeno‐associated virus (AAV) treatment inducing the overexpression of fibroblast growth factor 23 (FGF23), dietary intervention, as well as biosampling and tissue collection. (b) Quantification of plasma intact FGF23 (iFGF23) concentrations, serum phosphate (Pi), serum creatinine (Crea), and urinary albumin to creatinine ratio (ACR) in all three groups. (c) Representative images of the cortex of hematoxylin and eosin (HE), periodic acid‐Schiff (PAS), and picrosirius red stained kidney cross‐sections, as well as immunofluorescence (IF) staining of kidney injury molecule 1 (Kim‐1; orange) positive tubules. (d) Quantification of the scoring of tubular injury, of real‐time PCR analysis of Havcr1 , and of kidney fibrosis in the cortex. (e) Representative HE, PAS and picrosirius red staining focusing on the perivascular region of TLS development. (f) Representative IF costaining of CD45R + (green) and CD3 + (orange) lymphocytes, of CD45R (green) and Ki67 (orange), and of IgD (red) synthesis. (g) Quantification of lymphocytes using flow cytometry analysis of whole kidney tissue from mice of all three groups. (c, f) Counterstaining of cell nuclei using DAPI (blue). (c, e and f) Scale bars: 100 μm. (b, d, g) Data are presented as mean ± SD. One‐way analysis of variance (ANOVA) with Tukey's multiple comparisons test, * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. A, artery.
Figure Legend Snippet: High phosphate, not the increase of fibroblast growth factor 23 (FGF23), drives tubular injury and perivascular tertiary lymphoid structure (TLS) formation. (a) Schematic representation of the study design including specific time points for adeno‐associated virus (AAV) treatment inducing the overexpression of fibroblast growth factor 23 (FGF23), dietary intervention, as well as biosampling and tissue collection. (b) Quantification of plasma intact FGF23 (iFGF23) concentrations, serum phosphate (Pi), serum creatinine (Crea), and urinary albumin to creatinine ratio (ACR) in all three groups. (c) Representative images of the cortex of hematoxylin and eosin (HE), periodic acid‐Schiff (PAS), and picrosirius red stained kidney cross‐sections, as well as immunofluorescence (IF) staining of kidney injury molecule 1 (Kim‐1; orange) positive tubules. (d) Quantification of the scoring of tubular injury, of real‐time PCR analysis of Havcr1 , and of kidney fibrosis in the cortex. (e) Representative HE, PAS and picrosirius red staining focusing on the perivascular region of TLS development. (f) Representative IF costaining of CD45R + (green) and CD3 + (orange) lymphocytes, of CD45R (green) and Ki67 (orange), and of IgD (red) synthesis. (g) Quantification of lymphocytes using flow cytometry analysis of whole kidney tissue from mice of all three groups. (c, f) Counterstaining of cell nuclei using DAPI (blue). (c, e and f) Scale bars: 100 μm. (b, d, g) Data are presented as mean ± SD. One‐way analysis of variance (ANOVA) with Tukey's multiple comparisons test, * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. A, artery.

Techniques Used: Virus, Over Expression, Clinical Proteomics, Staining, Immunofluorescence, Real-time Polymerase Chain Reaction, Flow Cytometry

Elevated fibroblast growth factor 23 (FGF23) levels in hypophosphatemic mice do not cause kidney damage or promote the formation of tertiary lymphoid structures (TLS). (a) Schematic representation of the study design including time point for biosampling and tissue collection. (b) Quantification of plasma intact FGF23 (iFGF23) concentrations, serum phosphate (Pi), serum creatinine (Crea), and urinary albumin to creatinine ratio (ACR) in all three groups. (c) Representative images of the cortex of hematoxylin and eosin (HE), periodic acid‐Schiff (PAS), and picrosirius red stained kidney cross‐sections, as well as immunofluorescence (IF) staining of kidney injury molecule 1 (Kim‐1; orange) with DAPI (blue) counterstaining. Scale bars: 100 μm. (d) Quantification of the scoring of tubular injury, of real‐time PCR analysis of Havcr1 transcription, and of kidney fibrosis in the cortex. (b, d) Data are presented as mean ± SD. Unpaired t ‐tests with **** p < 0.0001.
Figure Legend Snippet: Elevated fibroblast growth factor 23 (FGF23) levels in hypophosphatemic mice do not cause kidney damage or promote the formation of tertiary lymphoid structures (TLS). (a) Schematic representation of the study design including time point for biosampling and tissue collection. (b) Quantification of plasma intact FGF23 (iFGF23) concentrations, serum phosphate (Pi), serum creatinine (Crea), and urinary albumin to creatinine ratio (ACR) in all three groups. (c) Representative images of the cortex of hematoxylin and eosin (HE), periodic acid‐Schiff (PAS), and picrosirius red stained kidney cross‐sections, as well as immunofluorescence (IF) staining of kidney injury molecule 1 (Kim‐1; orange) with DAPI (blue) counterstaining. Scale bars: 100 μm. (d) Quantification of the scoring of tubular injury, of real‐time PCR analysis of Havcr1 transcription, and of kidney fibrosis in the cortex. (b, d) Data are presented as mean ± SD. Unpaired t ‐tests with **** p < 0.0001.

Techniques Used: Clinical Proteomics, Staining, Immunofluorescence, Real-time Polymerase Chain Reaction



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Charles River Laboratories ifgf23 levels
High phosphate, not the increase of fibroblast growth factor 23 (FGF23), drives tubular injury and perivascular tertiary lymphoid structure (TLS) formation. (a) Schematic representation of the study design including specific time points for adeno‐associated virus (AAV) treatment inducing the overexpression of fibroblast growth factor 23 (FGF23), dietary intervention, as well as biosampling and tissue collection. (b) Quantification of plasma <t>intact</t> <t>FGF23</t> <t>(iFGF23)</t> concentrations, serum phosphate (Pi), serum creatinine (Crea), and urinary albumin to creatinine ratio (ACR) in all three groups. (c) Representative images of the cortex of hematoxylin and eosin (HE), periodic acid‐Schiff (PAS), and picrosirius red stained kidney cross‐sections, as well as immunofluorescence (IF) staining of kidney injury molecule 1 (Kim‐1; orange) positive tubules. (d) Quantification of the scoring of tubular injury, of real‐time PCR analysis of Havcr1 , and of kidney fibrosis in the cortex. (e) Representative HE, PAS and picrosirius red staining focusing on the perivascular region of TLS development. (f) Representative IF costaining of CD45R + (green) and CD3 + (orange) lymphocytes, of CD45R (green) and Ki67 (orange), and of IgD (red) synthesis. (g) Quantification of lymphocytes using flow cytometry analysis of whole kidney tissue from mice of all three groups. (c, f) Counterstaining of cell nuclei using DAPI (blue). (c, e and f) Scale bars: 100 μm. (b, d, g) Data are presented as mean ± SD. One‐way analysis of variance (ANOVA) with Tukey's multiple comparisons test, * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. A, artery.
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High phosphate, not the increase of fibroblast growth factor 23 (FGF23), drives tubular injury and perivascular tertiary lymphoid structure (TLS) formation. (a) Schematic representation of the study design including specific time points for adeno‐associated virus (AAV) treatment inducing the overexpression of fibroblast growth factor 23 (FGF23), dietary intervention, as well as biosampling and tissue collection. (b) Quantification of plasma intact FGF23 (iFGF23) concentrations, serum phosphate (Pi), serum creatinine (Crea), and urinary albumin to creatinine ratio (ACR) in all three groups. (c) Representative images of the cortex of hematoxylin and eosin (HE), periodic acid‐Schiff (PAS), and picrosirius red stained kidney cross‐sections, as well as immunofluorescence (IF) staining of kidney injury molecule 1 (Kim‐1; orange) positive tubules. (d) Quantification of the scoring of tubular injury, of real‐time PCR analysis of Havcr1 , and of kidney fibrosis in the cortex. (e) Representative HE, PAS and picrosirius red staining focusing on the perivascular region of TLS development. (f) Representative IF costaining of CD45R + (green) and CD3 + (orange) lymphocytes, of CD45R (green) and Ki67 (orange), and of IgD (red) synthesis. (g) Quantification of lymphocytes using flow cytometry analysis of whole kidney tissue from mice of all three groups. (c, f) Counterstaining of cell nuclei using DAPI (blue). (c, e and f) Scale bars: 100 μm. (b, d, g) Data are presented as mean ± SD. One‐way analysis of variance (ANOVA) with Tukey's multiple comparisons test, * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. A, artery.

Journal: The FASEB Journal

Article Title: High Phosphate Load Induces De Novo Formation of Tertiary Lymphoid Structures in the Kidney

doi: 10.1096/fj.202500968R

Figure Lengend Snippet: High phosphate, not the increase of fibroblast growth factor 23 (FGF23), drives tubular injury and perivascular tertiary lymphoid structure (TLS) formation. (a) Schematic representation of the study design including specific time points for adeno‐associated virus (AAV) treatment inducing the overexpression of fibroblast growth factor 23 (FGF23), dietary intervention, as well as biosampling and tissue collection. (b) Quantification of plasma intact FGF23 (iFGF23) concentrations, serum phosphate (Pi), serum creatinine (Crea), and urinary albumin to creatinine ratio (ACR) in all three groups. (c) Representative images of the cortex of hematoxylin and eosin (HE), periodic acid‐Schiff (PAS), and picrosirius red stained kidney cross‐sections, as well as immunofluorescence (IF) staining of kidney injury molecule 1 (Kim‐1; orange) positive tubules. (d) Quantification of the scoring of tubular injury, of real‐time PCR analysis of Havcr1 , and of kidney fibrosis in the cortex. (e) Representative HE, PAS and picrosirius red staining focusing on the perivascular region of TLS development. (f) Representative IF costaining of CD45R + (green) and CD3 + (orange) lymphocytes, of CD45R (green) and Ki67 (orange), and of IgD (red) synthesis. (g) Quantification of lymphocytes using flow cytometry analysis of whole kidney tissue from mice of all three groups. (c, f) Counterstaining of cell nuclei using DAPI (blue). (c, e and f) Scale bars: 100 μm. (b, d, g) Data are presented as mean ± SD. One‐way analysis of variance (ANOVA) with Tukey's multiple comparisons test, * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. A, artery.

Article Snippet: To specifically enhance circulating iFgf23 levels, 8‐week‐old male C57BL/6NCtrl mice (Charles River) received an adeno‐associated virus serotype 9 in which the full‐length cDNA of murine Fgf23 (AAV‐Fgf23) was subcloned as described previously [ ].

Techniques: Virus, Over Expression, Clinical Proteomics, Staining, Immunofluorescence, Real-time Polymerase Chain Reaction, Flow Cytometry

Elevated fibroblast growth factor 23 (FGF23) levels in hypophosphatemic mice do not cause kidney damage or promote the formation of tertiary lymphoid structures (TLS). (a) Schematic representation of the study design including time point for biosampling and tissue collection. (b) Quantification of plasma intact FGF23 (iFGF23) concentrations, serum phosphate (Pi), serum creatinine (Crea), and urinary albumin to creatinine ratio (ACR) in all three groups. (c) Representative images of the cortex of hematoxylin and eosin (HE), periodic acid‐Schiff (PAS), and picrosirius red stained kidney cross‐sections, as well as immunofluorescence (IF) staining of kidney injury molecule 1 (Kim‐1; orange) with DAPI (blue) counterstaining. Scale bars: 100 μm. (d) Quantification of the scoring of tubular injury, of real‐time PCR analysis of Havcr1 transcription, and of kidney fibrosis in the cortex. (b, d) Data are presented as mean ± SD. Unpaired t ‐tests with **** p < 0.0001.

Journal: The FASEB Journal

Article Title: High Phosphate Load Induces De Novo Formation of Tertiary Lymphoid Structures in the Kidney

doi: 10.1096/fj.202500968R

Figure Lengend Snippet: Elevated fibroblast growth factor 23 (FGF23) levels in hypophosphatemic mice do not cause kidney damage or promote the formation of tertiary lymphoid structures (TLS). (a) Schematic representation of the study design including time point for biosampling and tissue collection. (b) Quantification of plasma intact FGF23 (iFGF23) concentrations, serum phosphate (Pi), serum creatinine (Crea), and urinary albumin to creatinine ratio (ACR) in all three groups. (c) Representative images of the cortex of hematoxylin and eosin (HE), periodic acid‐Schiff (PAS), and picrosirius red stained kidney cross‐sections, as well as immunofluorescence (IF) staining of kidney injury molecule 1 (Kim‐1; orange) with DAPI (blue) counterstaining. Scale bars: 100 μm. (d) Quantification of the scoring of tubular injury, of real‐time PCR analysis of Havcr1 transcription, and of kidney fibrosis in the cortex. (b, d) Data are presented as mean ± SD. Unpaired t ‐tests with **** p < 0.0001.

Article Snippet: To specifically enhance circulating iFgf23 levels, 8‐week‐old male C57BL/6NCtrl mice (Charles River) received an adeno‐associated virus serotype 9 in which the full‐length cDNA of murine Fgf23 (AAV‐Fgf23) was subcloned as described previously [ ].

Techniques: Clinical Proteomics, Staining, Immunofluorescence, Real-time Polymerase Chain Reaction

WT and TG mice from (n=6-7 mice/group) were analyzed. Measured parameters include ( A ) serum phosphate, ( B ) serum intact iFGF23, and qPCR analysis of kidney tissue for ( C-G ) Slc34a1 and Slc34a3 ( encoding sodium-dependent phosphate transporters 2A and 2C), Cyp27b1 and Cyp24a1 ( encoding the enzymes that respectively generate and break down the active form of vitamin D, 1,25-dihydroxyvitamin D3) and Kl (encoding Klotho, the renal coreceptor for iFGF23). Data are mean ± SEM, analyzed by unpaired- t -test with Welch’s correction (two-tailed). *P <.05; ns = non-significant.

Journal: bioRxiv

Article Title: Transgenic augmentation of erythroferrone in mice ameliorates anemia in adenine-induced chronic kidney disease

doi: 10.1101/2024.12.06.627111

Figure Lengend Snippet: WT and TG mice from (n=6-7 mice/group) were analyzed. Measured parameters include ( A ) serum phosphate, ( B ) serum intact iFGF23, and qPCR analysis of kidney tissue for ( C-G ) Slc34a1 and Slc34a3 ( encoding sodium-dependent phosphate transporters 2A and 2C), Cyp27b1 and Cyp24a1 ( encoding the enzymes that respectively generate and break down the active form of vitamin D, 1,25-dihydroxyvitamin D3) and Kl (encoding Klotho, the renal coreceptor for iFGF23). Data are mean ± SEM, analyzed by unpaired- t -test with Welch’s correction (two-tailed). *P <.05; ns = non-significant.

Article Snippet: Intact bioactive FGF23 (iFGF23) levels were assessed by ELISA (60-6800, QuidelOrtho).

Techniques: Two Tailed Test