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customized rat kidney injury panel  (Meso Scale Diagnostics LLC)

 
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    Meso Scale Diagnostics LLC customized rat kidney injury panel
    Diabetic ZSF1 rats recapitulate phenotypic changes of DKD with marked disease improvement by sGC activators (A) Representation of the importance of heme-containing (native) sGC and heme-free (dysfunctional) form of sGC and its redox equilibrium. sGC stimulator efficacy depends on the ferrous, Fe(II), state of the heme group at the β subunit of sGC, while sGC activators bind directly to oxidized, Fe(III), or heme-free apo form of sGC. Similar to other cardiovascular disorders, DKD is associated with reduced NO bioavailability, increased oxidative stress, and endothelial dysfunction. cGMP, cyclic guanosine monophosphate; DKD, diabetic <t>kidney</t> disease; NO, nitric oxide; NOS, nitric oxide synthase; O 2 − , superoxide; ONOO − , peroxynitrite; sGCact, soluble guanylate cyclase activator; sGCstim, soluble guanylate cyclase stimulator. Adapted from Sandner et al. (B) Experimental ZSF1 <t>rat</t> model setup. sGCact, soluble guanylate cyclase activator; sGCstim, sGC stimulator. (C–E) Metabolic (serum cholesterol, glucose, and plasma HbA1c) (C), kidney function (D), and kidney <t>injury</t> markers (E) after 12 study weeks; p values are given for either one-way ANOVA or Kruskal-Wallis test (both Benjamini, Krieger, Yekutieli corrected). Ob, obese; ns, not significant. Color legend as in (B). (F) Histopathology changes in hematoxylin/eosin (left) and Sirius red/fast green (right) stained kidney sections. Scale bars, 500 μm. (G) Histopathology scoring; p values are given for Kruskal-Wallis test (Benjamini, Krieger, Yekutieli corrected). Color legend as in (B).
    Customized Rat Kidney Injury Panel, supplied by Meso Scale Diagnostics LLC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/customized+rat+kidney+injury+panel/pmc10140477-339-23-28?v=Meso+Scale+Diagnostics+LLC
    Average 90 stars, based on 1 article reviews
    customized rat kidney injury panel - by Bioz Stars, 2026-08
    90/100 stars

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    1) Product Images from "Treatment effects of soluble guanylate cyclase modulation on diabetic kidney disease at single-cell resolution"

    Article Title: Treatment effects of soluble guanylate cyclase modulation on diabetic kidney disease at single-cell resolution

    Journal: Cell Reports Medicine

    doi: 10.1016/j.xcrm.2023.100992

    Diabetic ZSF1 rats recapitulate phenotypic changes of DKD with marked disease improvement by sGC activators (A) Representation of the importance of heme-containing (native) sGC and heme-free (dysfunctional) form of sGC and its redox equilibrium. sGC stimulator efficacy depends on the ferrous, Fe(II), state of the heme group at the β subunit of sGC, while sGC activators bind directly to oxidized, Fe(III), or heme-free apo form of sGC. Similar to other cardiovascular disorders, DKD is associated with reduced NO bioavailability, increased oxidative stress, and endothelial dysfunction. cGMP, cyclic guanosine monophosphate; DKD, diabetic kidney disease; NO, nitric oxide; NOS, nitric oxide synthase; O 2 − , superoxide; ONOO − , peroxynitrite; sGCact, soluble guanylate cyclase activator; sGCstim, soluble guanylate cyclase stimulator. Adapted from Sandner et al. (B) Experimental ZSF1 rat model setup. sGCact, soluble guanylate cyclase activator; sGCstim, sGC stimulator. (C–E) Metabolic (serum cholesterol, glucose, and plasma HbA1c) (C), kidney function (D), and kidney injury markers (E) after 12 study weeks; p values are given for either one-way ANOVA or Kruskal-Wallis test (both Benjamini, Krieger, Yekutieli corrected). Ob, obese; ns, not significant. Color legend as in (B). (F) Histopathology changes in hematoxylin/eosin (left) and Sirius red/fast green (right) stained kidney sections. Scale bars, 500 μm. (G) Histopathology scoring; p values are given for Kruskal-Wallis test (Benjamini, Krieger, Yekutieli corrected). Color legend as in (B).
    Figure Legend Snippet: Diabetic ZSF1 rats recapitulate phenotypic changes of DKD with marked disease improvement by sGC activators (A) Representation of the importance of heme-containing (native) sGC and heme-free (dysfunctional) form of sGC and its redox equilibrium. sGC stimulator efficacy depends on the ferrous, Fe(II), state of the heme group at the β subunit of sGC, while sGC activators bind directly to oxidized, Fe(III), or heme-free apo form of sGC. Similar to other cardiovascular disorders, DKD is associated with reduced NO bioavailability, increased oxidative stress, and endothelial dysfunction. cGMP, cyclic guanosine monophosphate; DKD, diabetic kidney disease; NO, nitric oxide; NOS, nitric oxide synthase; O 2 − , superoxide; ONOO − , peroxynitrite; sGCact, soluble guanylate cyclase activator; sGCstim, soluble guanylate cyclase stimulator. Adapted from Sandner et al. (B) Experimental ZSF1 rat model setup. sGCact, soluble guanylate cyclase activator; sGCstim, sGC stimulator. (C–E) Metabolic (serum cholesterol, glucose, and plasma HbA1c) (C), kidney function (D), and kidney injury markers (E) after 12 study weeks; p values are given for either one-way ANOVA or Kruskal-Wallis test (both Benjamini, Krieger, Yekutieli corrected). Ob, obese; ns, not significant. Color legend as in (B). (F) Histopathology changes in hematoxylin/eosin (left) and Sirius red/fast green (right) stained kidney sections. Scale bars, 500 μm. (G) Histopathology scoring; p values are given for Kruskal-Wallis test (Benjamini, Krieger, Yekutieli corrected). Color legend as in (B).

    Techniques Used: Clinical Proteomics, Histopathology, Staining



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    Diabetic ZSF1 rats recapitulate phenotypic changes of DKD with marked disease improvement by sGC activators (A) Representation of the importance of heme-containing (native) sGC and heme-free (dysfunctional) form of sGC and its redox equilibrium. sGC stimulator efficacy depends on the ferrous, Fe(II), state of the heme group at the β subunit of sGC, while sGC activators bind directly to oxidized, Fe(III), or heme-free apo form of sGC. Similar to other cardiovascular disorders, DKD is associated with reduced NO bioavailability, increased oxidative stress, and endothelial dysfunction. cGMP, cyclic guanosine monophosphate; DKD, diabetic <t>kidney</t> disease; NO, nitric oxide; NOS, nitric oxide synthase; O 2 − , superoxide; ONOO − , peroxynitrite; sGCact, soluble guanylate cyclase activator; sGCstim, soluble guanylate cyclase stimulator. Adapted from Sandner et al. (B) Experimental ZSF1 <t>rat</t> model setup. sGCact, soluble guanylate cyclase activator; sGCstim, sGC stimulator. (C–E) Metabolic (serum cholesterol, glucose, and plasma HbA1c) (C), kidney function (D), and kidney <t>injury</t> markers (E) after 12 study weeks; p values are given for either one-way ANOVA or Kruskal-Wallis test (both Benjamini, Krieger, Yekutieli corrected). Ob, obese; ns, not significant. Color legend as in (B). (F) Histopathology changes in hematoxylin/eosin (left) and Sirius red/fast green (right) stained kidney sections. Scale bars, 500 μm. (G) Histopathology scoring; p values are given for Kruskal-Wallis test (Benjamini, Krieger, Yekutieli corrected). Color legend as in (B).
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    Diabetic ZSF1 rats recapitulate phenotypic changes of DKD with marked disease improvement by sGC activators (A) Representation of the importance of heme-containing (native) sGC and heme-free (dysfunctional) form of sGC and its redox equilibrium. sGC stimulator efficacy depends on the ferrous, Fe(II), state of the heme group at the β subunit of sGC, while sGC activators bind directly to oxidized, Fe(III), or heme-free apo form of sGC. Similar to other cardiovascular disorders, DKD is associated with reduced NO bioavailability, increased oxidative stress, and endothelial dysfunction. cGMP, cyclic guanosine monophosphate; DKD, diabetic <t>kidney</t> disease; NO, nitric oxide; NOS, nitric oxide synthase; O 2 − , superoxide; ONOO − , peroxynitrite; sGCact, soluble guanylate cyclase activator; sGCstim, soluble guanylate cyclase stimulator. Adapted from Sandner et al. (B) Experimental ZSF1 <t>rat</t> model setup. sGCact, soluble guanylate cyclase activator; sGCstim, sGC stimulator. (C–E) Metabolic (serum cholesterol, glucose, and plasma HbA1c) (C), kidney function (D), and kidney <t>injury</t> markers (E) after 12 study weeks; p values are given for either one-way ANOVA or Kruskal-Wallis test (both Benjamini, Krieger, Yekutieli corrected). Ob, obese; ns, not significant. Color legend as in (B). (F) Histopathology changes in hematoxylin/eosin (left) and Sirius red/fast green (right) stained kidney sections. Scale bars, 500 μm. (G) Histopathology scoring; p values are given for Kruskal-Wallis test (Benjamini, Krieger, Yekutieli corrected). Color legend as in (B).
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    Diabetic ZSF1 rats recapitulate phenotypic changes of DKD with marked disease improvement by sGC activators (A) Representation of the importance of heme-containing (native) sGC and heme-free (dysfunctional) form of sGC and its redox equilibrium. sGC stimulator efficacy depends on the ferrous, Fe(II), state of the heme group at the β subunit of sGC, while sGC activators bind directly to oxidized, Fe(III), or heme-free apo form of sGC. Similar to other cardiovascular disorders, DKD is associated with reduced NO bioavailability, increased oxidative stress, and endothelial dysfunction. cGMP, cyclic guanosine monophosphate; DKD, diabetic kidney disease; NO, nitric oxide; NOS, nitric oxide synthase; O 2 − , superoxide; ONOO − , peroxynitrite; sGCact, soluble guanylate cyclase activator; sGCstim, soluble guanylate cyclase stimulator. Adapted from Sandner et al. (B) Experimental ZSF1 rat model setup. sGCact, soluble guanylate cyclase activator; sGCstim, sGC stimulator. (C–E) Metabolic (serum cholesterol, glucose, and plasma HbA1c) (C), kidney function (D), and kidney injury markers (E) after 12 study weeks; p values are given for either one-way ANOVA or Kruskal-Wallis test (both Benjamini, Krieger, Yekutieli corrected). Ob, obese; ns, not significant. Color legend as in (B). (F) Histopathology changes in hematoxylin/eosin (left) and Sirius red/fast green (right) stained kidney sections. Scale bars, 500 μm. (G) Histopathology scoring; p values are given for Kruskal-Wallis test (Benjamini, Krieger, Yekutieli corrected). Color legend as in (B).

    Journal: Cell Reports Medicine

    Article Title: Treatment effects of soluble guanylate cyclase modulation on diabetic kidney disease at single-cell resolution

    doi: 10.1016/j.xcrm.2023.100992

    Figure Lengend Snippet: Diabetic ZSF1 rats recapitulate phenotypic changes of DKD with marked disease improvement by sGC activators (A) Representation of the importance of heme-containing (native) sGC and heme-free (dysfunctional) form of sGC and its redox equilibrium. sGC stimulator efficacy depends on the ferrous, Fe(II), state of the heme group at the β subunit of sGC, while sGC activators bind directly to oxidized, Fe(III), or heme-free apo form of sGC. Similar to other cardiovascular disorders, DKD is associated with reduced NO bioavailability, increased oxidative stress, and endothelial dysfunction. cGMP, cyclic guanosine monophosphate; DKD, diabetic kidney disease; NO, nitric oxide; NOS, nitric oxide synthase; O 2 − , superoxide; ONOO − , peroxynitrite; sGCact, soluble guanylate cyclase activator; sGCstim, soluble guanylate cyclase stimulator. Adapted from Sandner et al. (B) Experimental ZSF1 rat model setup. sGCact, soluble guanylate cyclase activator; sGCstim, sGC stimulator. (C–E) Metabolic (serum cholesterol, glucose, and plasma HbA1c) (C), kidney function (D), and kidney injury markers (E) after 12 study weeks; p values are given for either one-way ANOVA or Kruskal-Wallis test (both Benjamini, Krieger, Yekutieli corrected). Ob, obese; ns, not significant. Color legend as in (B). (F) Histopathology changes in hematoxylin/eosin (left) and Sirius red/fast green (right) stained kidney sections. Scale bars, 500 μm. (G) Histopathology scoring; p values are given for Kruskal-Wallis test (Benjamini, Krieger, Yekutieli corrected). Color legend as in (B).

    Article Snippet: With regard to biomarkers, all assays were performed according to manufacturers’ instructions: Plasma KIM-1 and neutrophil gelatinase-associated lipocalin (NGAL) were measured using a customized Rat Kidney Injury Panel (Meso Scale Discovery).

    Techniques: Clinical Proteomics, Histopathology, Staining