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Structured Review

Polysciences inc picrosirius red stain kit
A. Schematic outlining the generation of myofiber-specific Dystrophin conditional knockout mice ( Dmd :HSA KO) by breeding our Dmd flox52 /Y mice to human skeletal actin ( HSA )-Cre transgenic mice. Cre-mediated excision of Dmd exon 52 results in an out-of-frame disruption and instability of the Dp427 RNA transcript. B. Western immunoblotting for the large Dp427m protein in the TA and soleus muscles of WT (open), Dmd flox52 /Y (blue), mdx 5cv (red), and Dmd :HSA KO (green) adult (6-month-old) male mice. C. Densitometry graphs WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO immunoblots taken from TA and soleus muscle lysates and normalized to Vinculin protein. N = 5 separate mice per cohort. D. Histochemical staining of TA, soleus, and diaphragm muscles isolated from the WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO male mice. Hematoxylin and eosin (H&E), <t>picrosirius</t> red, and Masson’s trichrome histochemical staining performed. Scale bar = 100 µm. E. Percent fibrosis (%) in the TA muscles of the four mouse cohorts analyzed. F. Percentage (%) centralized myonuclei for the approximately 600 myofibers of the TA muscles of the four mouse cohorts analyzed. G. Cross-sectional area (CSA) displaying myofiber sizes (µm 2 ) shown for each of the four cohorts. Two-way ANOVA with Bonferroni correction performed. P-values of significance are shown: * p < 0.05, ** p < 0.01, *** p < 0.005, and **** p < 0.001.
Picrosirius Red Stain Kit, supplied by Polysciences inc, 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/picrosirius+red+stain+kit/bio_rxiv__2025__01__30__635777-118-25-29?v=Polysciences+inc
Average 90 stars, based on 1 article reviews
picrosirius red stain kit - by Bioz Stars, 2026-08
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Images

1) Product Images from "Conditional Dystrophin ablation causes profound effects on muscle development, neurobehavior, and extracellular matrix pathways"

Article Title: Conditional Dystrophin ablation causes profound effects on muscle development, neurobehavior, and extracellular matrix pathways

Journal: bioRxiv

doi: 10.1101/2025.01.30.635777

A. Schematic outlining the generation of myofiber-specific Dystrophin conditional knockout mice ( Dmd :HSA KO) by breeding our Dmd flox52 /Y mice to human skeletal actin ( HSA )-Cre transgenic mice. Cre-mediated excision of Dmd exon 52 results in an out-of-frame disruption and instability of the Dp427 RNA transcript. B. Western immunoblotting for the large Dp427m protein in the TA and soleus muscles of WT (open), Dmd flox52 /Y (blue), mdx 5cv (red), and Dmd :HSA KO (green) adult (6-month-old) male mice. C. Densitometry graphs WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO immunoblots taken from TA and soleus muscle lysates and normalized to Vinculin protein. N = 5 separate mice per cohort. D. Histochemical staining of TA, soleus, and diaphragm muscles isolated from the WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO male mice. Hematoxylin and eosin (H&E), picrosirius red, and Masson’s trichrome histochemical staining performed. Scale bar = 100 µm. E. Percent fibrosis (%) in the TA muscles of the four mouse cohorts analyzed. F. Percentage (%) centralized myonuclei for the approximately 600 myofibers of the TA muscles of the four mouse cohorts analyzed. G. Cross-sectional area (CSA) displaying myofiber sizes (µm 2 ) shown for each of the four cohorts. Two-way ANOVA with Bonferroni correction performed. P-values of significance are shown: * p < 0.05, ** p < 0.01, *** p < 0.005, and **** p < 0.001.
Figure Legend Snippet: A. Schematic outlining the generation of myofiber-specific Dystrophin conditional knockout mice ( Dmd :HSA KO) by breeding our Dmd flox52 /Y mice to human skeletal actin ( HSA )-Cre transgenic mice. Cre-mediated excision of Dmd exon 52 results in an out-of-frame disruption and instability of the Dp427 RNA transcript. B. Western immunoblotting for the large Dp427m protein in the TA and soleus muscles of WT (open), Dmd flox52 /Y (blue), mdx 5cv (red), and Dmd :HSA KO (green) adult (6-month-old) male mice. C. Densitometry graphs WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO immunoblots taken from TA and soleus muscle lysates and normalized to Vinculin protein. N = 5 separate mice per cohort. D. Histochemical staining of TA, soleus, and diaphragm muscles isolated from the WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO male mice. Hematoxylin and eosin (H&E), picrosirius red, and Masson’s trichrome histochemical staining performed. Scale bar = 100 µm. E. Percent fibrosis (%) in the TA muscles of the four mouse cohorts analyzed. F. Percentage (%) centralized myonuclei for the approximately 600 myofibers of the TA muscles of the four mouse cohorts analyzed. G. Cross-sectional area (CSA) displaying myofiber sizes (µm 2 ) shown for each of the four cohorts. Two-way ANOVA with Bonferroni correction performed. P-values of significance are shown: * p < 0.05, ** p < 0.01, *** p < 0.005, and **** p < 0.001.

Techniques Used: Knock-Out, Transgenic Assay, Disruption, Western Blot, Muscles, Staining, Isolation



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A. Schematic outlining the generation of myofiber-specific Dystrophin conditional knockout mice ( Dmd :HSA KO) by breeding our Dmd flox52 /Y mice to human skeletal actin ( HSA )-Cre transgenic mice. Cre-mediated excision of Dmd exon 52 results in an out-of-frame disruption and instability of the Dp427 RNA transcript. B. Western immunoblotting for the large Dp427m protein in the TA and soleus muscles of WT (open), Dmd flox52 /Y (blue), mdx 5cv (red), and Dmd :HSA KO (green) adult (6-month-old) male mice. C. Densitometry graphs WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO immunoblots taken from TA and soleus muscle lysates and normalized to Vinculin protein. N = 5 separate mice per cohort. D. Histochemical staining of TA, soleus, and diaphragm muscles isolated from the WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO male mice. Hematoxylin and eosin (H&E), <t>picrosirius</t> red, and Masson’s trichrome histochemical staining performed. Scale bar = 100 µm. E. Percent fibrosis (%) in the TA muscles of the four mouse cohorts analyzed. F. Percentage (%) centralized myonuclei for the approximately 600 myofibers of the TA muscles of the four mouse cohorts analyzed. G. Cross-sectional area (CSA) displaying myofiber sizes (µm 2 ) shown for each of the four cohorts. Two-way ANOVA with Bonferroni correction performed. P-values of significance are shown: * p < 0.05, ** p < 0.01, *** p < 0.005, and **** p < 0.001.
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Image Search Results


LOX inhibitor improves MIA-induced joint damage (A) Representative images of H&E staining of rat joint tissues across four groups. Scale bars, 200 μm, n = 4. (B) Picrosirius red staining images of rat joint tissues across four groups. Scale bars, 100 μm. (C–F) Immunohistochemistry of LOX, IL-1β, MFAP5, and FBN1, rat joint tissues across four groups. IOD, integrated optical density. Scale bars, 400 μm, n = 4. Data were presented as mean ± SEM. Statistical significance was calculated using one-way ANOVA followed by Tukey’s multiple comparisons test (A and C–F). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: iScience

Article Title: MFAP5 + synovial fibroblasts drive LOX upregulation to promote osteoarthritis progression

doi: 10.1016/j.isci.2026.116286

Figure Lengend Snippet: LOX inhibitor improves MIA-induced joint damage (A) Representative images of H&E staining of rat joint tissues across four groups. Scale bars, 200 μm, n = 4. (B) Picrosirius red staining images of rat joint tissues across four groups. Scale bars, 100 μm. (C–F) Immunohistochemistry of LOX, IL-1β, MFAP5, and FBN1, rat joint tissues across four groups. IOD, integrated optical density. Scale bars, 400 μm, n = 4. Data were presented as mean ± SEM. Statistical significance was calculated using one-way ANOVA followed by Tukey’s multiple comparisons test (A and C–F). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Picrosirius red staining Kit , Servicebio , Cat# G1078.

Techniques: Staining, Immunohistochemistry

A. Schematic outlining the generation of myofiber-specific Dystrophin conditional knockout mice ( Dmd :HSA KO) by breeding our Dmd flox52 /Y mice to human skeletal actin ( HSA )-Cre transgenic mice. Cre-mediated excision of Dmd exon 52 results in an out-of-frame disruption and instability of the Dp427 RNA transcript. B. Western immunoblotting for the large Dp427m protein in the TA and soleus muscles of WT (open), Dmd flox52 /Y (blue), mdx 5cv (red), and Dmd :HSA KO (green) adult (6-month-old) male mice. C. Densitometry graphs WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO immunoblots taken from TA and soleus muscle lysates and normalized to Vinculin protein. N = 5 separate mice per cohort. D. Histochemical staining of TA, soleus, and diaphragm muscles isolated from the WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO male mice. Hematoxylin and eosin (H&E), picrosirius red, and Masson’s trichrome histochemical staining performed. Scale bar = 100 µm. E. Percent fibrosis (%) in the TA muscles of the four mouse cohorts analyzed. F. Percentage (%) centralized myonuclei for the approximately 600 myofibers of the TA muscles of the four mouse cohorts analyzed. G. Cross-sectional area (CSA) displaying myofiber sizes (µm 2 ) shown for each of the four cohorts. Two-way ANOVA with Bonferroni correction performed. P-values of significance are shown: * p < 0.05, ** p < 0.01, *** p < 0.005, and **** p < 0.001.

Journal: bioRxiv

Article Title: Conditional Dystrophin ablation causes profound effects on muscle development, neurobehavior, and extracellular matrix pathways

doi: 10.1101/2025.01.30.635777

Figure Lengend Snippet: A. Schematic outlining the generation of myofiber-specific Dystrophin conditional knockout mice ( Dmd :HSA KO) by breeding our Dmd flox52 /Y mice to human skeletal actin ( HSA )-Cre transgenic mice. Cre-mediated excision of Dmd exon 52 results in an out-of-frame disruption and instability of the Dp427 RNA transcript. B. Western immunoblotting for the large Dp427m protein in the TA and soleus muscles of WT (open), Dmd flox52 /Y (blue), mdx 5cv (red), and Dmd :HSA KO (green) adult (6-month-old) male mice. C. Densitometry graphs WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO immunoblots taken from TA and soleus muscle lysates and normalized to Vinculin protein. N = 5 separate mice per cohort. D. Histochemical staining of TA, soleus, and diaphragm muscles isolated from the WT, Dmd flox52 /Y , mdx 5cv , and Dmd :HSA KO male mice. Hematoxylin and eosin (H&E), picrosirius red, and Masson’s trichrome histochemical staining performed. Scale bar = 100 µm. E. Percent fibrosis (%) in the TA muscles of the four mouse cohorts analyzed. F. Percentage (%) centralized myonuclei for the approximately 600 myofibers of the TA muscles of the four mouse cohorts analyzed. G. Cross-sectional area (CSA) displaying myofiber sizes (µm 2 ) shown for each of the four cohorts. Two-way ANOVA with Bonferroni correction performed. P-values of significance are shown: * p < 0.05, ** p < 0.01, *** p < 0.005, and **** p < 0.001.

Article Snippet: Masson’s trichrome staining was performed using a Masson’s Trichrome Stain Kit (Polysciences, Inc; Warrington, PA; Cat# 25088-1) and picrosirius red staining was performed using a Picrosirius Red Stain Kit (Polysciences, Inc; Cat# 24901-500).

Techniques: Knock-Out, Transgenic Assay, Disruption, Western Blot, Muscles, Staining, Isolation