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AAV‐mediated delivery of circIdh2 or circIdh2‐aa attenuated myocardial fibrosis and EndMT‐related marker changes in vivo. (A) HE staining of myocardial infarction tissues from the sham, model, circIdh2‐AAV, and circIdh2‐aa‐AAV groups. (B) Masson staining of MI tissues. (C) IF detection and quantification of fibrotic markers (Collagen I and TGF‐ β ) in myocardial tissues. Scale bars, 100 μ m. (D) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin). Data are mean ± SD; n = 3 rats per group; one‐way ANOVA; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
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AAV‐mediated delivery of circIdh2 or circIdh2‐aa attenuated myocardial fibrosis and EndMT‐related marker changes in vivo. (A) HE staining of myocardial infarction tissues from the sham, model, circIdh2‐AAV, and circIdh2‐aa‐AAV groups. (B) Masson staining of MI tissues. (C) IF detection and quantification of fibrotic markers (Collagen I and TGF‐ β ) in myocardial tissues. Scale bars, 100 μ m. (D) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin). Data are mean ± SD; n = 3 rats per group; one‐way ANOVA; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
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AAV‐mediated delivery of circIdh2 or circIdh2‐aa attenuated myocardial fibrosis and EndMT‐related marker changes in vivo. (A) HE staining of myocardial infarction tissues from the sham, model, circIdh2‐AAV, and circIdh2‐aa‐AAV groups. (B) Masson staining of MI tissues. (C) IF detection and quantification of fibrotic markers (Collagen I and TGF‐ β ) in myocardial tissues. Scale bars, 100 μ m. (D) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin). Data are mean ± SD; n = 3 rats per group; one‐way ANOVA; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
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AAV‐mediated delivery of circIdh2 or circIdh2‐aa attenuated myocardial fibrosis and EndMT‐related marker changes in vivo. (A) HE staining of myocardial infarction tissues from the sham, model, circIdh2‐AAV, and circIdh2‐aa‐AAV groups. (B) Masson staining of MI tissues. (C) IF detection and quantification of fibrotic markers (Collagen I and TGF‐ β ) in myocardial tissues. Scale bars, 100 μ m. (D) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin). Data are mean ± SD; n = 3 rats per group; one‐way ANOVA; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
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AAV‐mediated delivery of circIdh2 or circIdh2‐aa attenuated myocardial fibrosis and EndMT‐related marker changes in vivo. (A) HE staining of myocardial infarction tissues from the sham, model, circIdh2‐AAV, and circIdh2‐aa‐AAV groups. (B) Masson staining of MI tissues. (C) IF detection and quantification of fibrotic markers (Collagen I and TGF‐ β ) in myocardial tissues. Scale bars, 100 μ m. (D) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin). Data are mean ± SD; n = 3 rats per group; one‐way ANOVA; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
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AAV‐mediated delivery of circIdh2 or circIdh2‐aa attenuated myocardial fibrosis and EndMT‐related marker changes in vivo. (A) HE staining of myocardial infarction tissues from the sham, model, circIdh2‐AAV, and circIdh2‐aa‐AAV groups. (B) Masson staining of MI tissues. (C) IF detection and quantification of fibrotic markers (Collagen I and TGF‐ β ) in myocardial tissues. Scale bars, 100 μ m. (D) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin). Data are mean ± SD; n = 3 rats per group; one‐way ANOVA; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.
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MI induces atrial fibrosis and upregulates the EZH2/H3K27me3 signaling in mice . (A,B) Representative Masson staining images (A) and quantitative analysis (B) of atrial fibrosis in the sham and MI groups ( n = 5). Scale bar = 0.04 mm under 20× field of view. (C–E) Western blot analysis and quantitative analysis of the expression levels of collagen I, α-SMA, and TGF-β1 in the atria of mice from the Sham and MI groups ( n = 6). (F) qPCR analysis of the expression levels of Ezh2 mRNA in the atria of mice from the Sham and MI groups ( n = 6). (G,H) Western blot analysis and quantitative analysis of the expression levels of EZH2 ( n = 6) and H3K27me3 ( n = 9) in the atria of mice from the Sham and MI groups. Sham, Sham operation group; MI, myocardial infarction group; α-SMA, alpha-smooth muscle actin; TGF-β1, transforming growth factor-beta1; EZH2, Enhancer of Zeste Homolog 2; H3K27me3, trimethylated Histone H3 at Lysine 27. Values are displayed as mean ± standard error of the mean.
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MI induces atrial fibrosis and upregulates the EZH2/H3K27me3 signaling in mice . (A,B) Representative Masson staining images (A) and quantitative analysis (B) of atrial fibrosis in the sham and MI groups ( n = 5). Scale bar = 0.04 mm under 20× field of view. (C–E) Western blot analysis and quantitative analysis of the expression levels of collagen I, α-SMA, and TGF-β1 in the atria of mice from the Sham and MI groups ( n = 6). (F) qPCR analysis of the expression levels of Ezh2 mRNA in the atria of mice from the Sham and MI groups ( n = 6). (G,H) Western blot analysis and quantitative analysis of the expression levels of EZH2 ( n = 6) and H3K27me3 ( n = 9) in the atria of mice from the Sham and MI groups. Sham, Sham operation group; MI, myocardial infarction group; α-SMA, alpha-smooth muscle actin; TGF-β1, transforming growth factor-beta1; EZH2, Enhancer of Zeste Homolog 2; H3K27me3, trimethylated Histone H3 at Lysine 27. Values are displayed as mean ± standard error of the mean.
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Image Search Results


AAV‐mediated delivery of circIdh2 or circIdh2‐aa attenuated myocardial fibrosis and EndMT‐related marker changes in vivo. (A) HE staining of myocardial infarction tissues from the sham, model, circIdh2‐AAV, and circIdh2‐aa‐AAV groups. (B) Masson staining of MI tissues. (C) IF detection and quantification of fibrotic markers (Collagen I and TGF‐ β ) in myocardial tissues. Scale bars, 100 μ m. (D) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin). Data are mean ± SD; n = 3 rats per group; one‐way ANOVA; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: AAV‐mediated delivery of circIdh2 or circIdh2‐aa attenuated myocardial fibrosis and EndMT‐related marker changes in vivo. (A) HE staining of myocardial infarction tissues from the sham, model, circIdh2‐AAV, and circIdh2‐aa‐AAV groups. (B) Masson staining of MI tissues. (C) IF detection and quantification of fibrotic markers (Collagen I and TGF‐ β ) in myocardial tissues. Scale bars, 100 μ m. (D) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin). Data are mean ± SD; n = 3 rats per group; one‐way ANOVA; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The sections were then incubated overnight at 4°C with primary antibodies against Collagen I (1:200, #66761‐1‐Ig, Proteintech) and TGF‐ β 1 (1:200, #81746‐2‐RR, Proteintech).

Techniques: Marker, In Vivo, H&E Stain, Staining, Western Blot, Analysis

MI induces atrial fibrosis and upregulates the EZH2/H3K27me3 signaling in mice . (A,B) Representative Masson staining images (A) and quantitative analysis (B) of atrial fibrosis in the sham and MI groups ( n = 5). Scale bar = 0.04 mm under 20× field of view. (C–E) Western blot analysis and quantitative analysis of the expression levels of collagen I, α-SMA, and TGF-β1 in the atria of mice from the Sham and MI groups ( n = 6). (F) qPCR analysis of the expression levels of Ezh2 mRNA in the atria of mice from the Sham and MI groups ( n = 6). (G,H) Western blot analysis and quantitative analysis of the expression levels of EZH2 ( n = 6) and H3K27me3 ( n = 9) in the atria of mice from the Sham and MI groups. Sham, Sham operation group; MI, myocardial infarction group; α-SMA, alpha-smooth muscle actin; TGF-β1, transforming growth factor-beta1; EZH2, Enhancer of Zeste Homolog 2; H3K27me3, trimethylated Histone H3 at Lysine 27. Values are displayed as mean ± standard error of the mean.

Journal: Reviews in Cardiovascular Medicine

Article Title: Enhancer of Zeste Homolog 2 Inhibition Attenuates Atrial Fibrillation Post-Myocardial Infarction Through Reduced Atrial Fibrosis

doi: 10.31083/RCM51343

Figure Lengend Snippet: MI induces atrial fibrosis and upregulates the EZH2/H3K27me3 signaling in mice . (A,B) Representative Masson staining images (A) and quantitative analysis (B) of atrial fibrosis in the sham and MI groups ( n = 5). Scale bar = 0.04 mm under 20× field of view. (C–E) Western blot analysis and quantitative analysis of the expression levels of collagen I, α-SMA, and TGF-β1 in the atria of mice from the Sham and MI groups ( n = 6). (F) qPCR analysis of the expression levels of Ezh2 mRNA in the atria of mice from the Sham and MI groups ( n = 6). (G,H) Western blot analysis and quantitative analysis of the expression levels of EZH2 ( n = 6) and H3K27me3 ( n = 9) in the atria of mice from the Sham and MI groups. Sham, Sham operation group; MI, myocardial infarction group; α-SMA, alpha-smooth muscle actin; TGF-β1, transforming growth factor-beta1; EZH2, Enhancer of Zeste Homolog 2; H3K27me3, trimethylated Histone H3 at Lysine 27. Values are displayed as mean ± standard error of the mean.

Article Snippet: The antibodies utilized in this study comprised the following: Enhancer of Zeste Homolog 2 (EZH2, 5246S, CST, USA), trimethylated Histone H3 at Lysine 27 (H3K27me3, 9733S, CST, USA), Histone 3 (H3, 9715S, CST, USA), collagen I (14695-1-AP, Proteintech, USA), Transforming Growth Factor-beta1 (TGF-β1, 81746-2-RR, Proteintech, USA), Alpha-Smooth Muscle Actin (α-SMA, 14395-1-AP, Proteintech, USA), and Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH, 60004-1-lg, Proteintech, USA).

Techniques: Staining, Analysis, Western Blot, Expressing

Inhibition of EZH2 attenuates atrial fibrosis post-MI . (A,B) Representative Masson staining images (A) and quantitative analysis (B) of atrial fibrosis in the MI + Vehicle and MI + GSK126 groups ( n = 5). Scale bar = 0.04 mm under 20× field of view. (C–E) Western blot analysis and quantitative analysis of the expression levels of collagen I, α-SMA, and TGF-β1 in the atria of mice from the MI + Vehicle and MI + GSK126 groups ( n = 6). MI + Vehicle, myocardial infarction with vehicle control group; MI + GSK126, myocardial infarction group treated with GSK126; EZH2, Enhancer of Zeste Homolog 2; α-SMA, alpha-smooth muscle actin; TGF-β1, transforming growth factor-beta1. Values are displayed as mean ± standard error of the mean.

Journal: Reviews in Cardiovascular Medicine

Article Title: Enhancer of Zeste Homolog 2 Inhibition Attenuates Atrial Fibrillation Post-Myocardial Infarction Through Reduced Atrial Fibrosis

doi: 10.31083/RCM51343

Figure Lengend Snippet: Inhibition of EZH2 attenuates atrial fibrosis post-MI . (A,B) Representative Masson staining images (A) and quantitative analysis (B) of atrial fibrosis in the MI + Vehicle and MI + GSK126 groups ( n = 5). Scale bar = 0.04 mm under 20× field of view. (C–E) Western blot analysis and quantitative analysis of the expression levels of collagen I, α-SMA, and TGF-β1 in the atria of mice from the MI + Vehicle and MI + GSK126 groups ( n = 6). MI + Vehicle, myocardial infarction with vehicle control group; MI + GSK126, myocardial infarction group treated with GSK126; EZH2, Enhancer of Zeste Homolog 2; α-SMA, alpha-smooth muscle actin; TGF-β1, transforming growth factor-beta1. Values are displayed as mean ± standard error of the mean.

Article Snippet: The antibodies utilized in this study comprised the following: Enhancer of Zeste Homolog 2 (EZH2, 5246S, CST, USA), trimethylated Histone H3 at Lysine 27 (H3K27me3, 9733S, CST, USA), Histone 3 (H3, 9715S, CST, USA), collagen I (14695-1-AP, Proteintech, USA), Transforming Growth Factor-beta1 (TGF-β1, 81746-2-RR, Proteintech, USA), Alpha-Smooth Muscle Actin (α-SMA, 14395-1-AP, Proteintech, USA), and Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH, 60004-1-lg, Proteintech, USA).

Techniques: Inhibition, Staining, Analysis, Western Blot, Expressing, Control