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mouse anti platelet endothelial cell adhesion molecule 1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc mouse anti platelet endothelial cell adhesion molecule 1
    Mouse Anti Platelet Endothelial Cell Adhesion Molecule 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1457 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti+platelet+endothelial+cell+adhesion+molecule+1/pm41177181-128-23-33?v=Cell+Signaling+Technology+Inc
    Average 96 stars, based on 1457 article reviews
    mouse anti platelet endothelial cell adhesion molecule 1 - by Bioz Stars, 2026-08
    96/100 stars

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    Becton Dickinson rat anti-mouse cd31 (platelet endothelial cell adhesion molecule, pecam-1) antibody
    Intramyocardial injection of IL-10 enhances revascularization in the ischemic myocardium. Long-term revascularization, including angiogenesis and vasculogenesis, in the ischemic myocardium was evaluated by the presence of <t>CD31</t> + endothelial cells (ECs) and αSMA + peri-vascular smooth muscle cells (SMCs), respectively, at 6 weeks post-infarction ( n = 3 per group). Perivascular SMCs defined as αSMA + cells around CD31 + ECs. Healthy (normal) hearts served as baseline controls ( n = 3). (A) Representative images of CD31 + ECs (red) and αSMA + SMCs (green) within the infarct region at the mid-infarct level from each group (scale bars: 50 μm). Nuclei were stained in blue. (B) Quantitatively, only the 250 ng group had a significantly higher density of CD31 + ECs at the infarct (p = 0.013, vs saline). (C) No significant difference in the CD31 + EC density was noted in the peri-infarct area (all p > 0.05, vs saline). (D) Only the 1,000 group had a significantly higher density of αSMA + SMCs within the infarct region (p = 0.045, vs saline). (E) No notable difference in the αSMA + SMC density in the peri-infarct area (all p > 0.05, vs saline). Note: *p < 0.05.
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    Cell Signaling Technology Inc anti platelet endothelial cell adhesion molecule 1 cd31
    Intramyocardial injection of IL-10 enhances revascularization in the ischemic myocardium. Long-term revascularization, including angiogenesis and vasculogenesis, in the ischemic myocardium was evaluated by the presence of <t>CD31</t> + endothelial cells (ECs) and αSMA + peri-vascular smooth muscle cells (SMCs), respectively, at 6 weeks post-infarction ( n = 3 per group). Perivascular SMCs defined as αSMA + cells around CD31 + ECs. Healthy (normal) hearts served as baseline controls ( n = 3). (A) Representative images of CD31 + ECs (red) and αSMA + SMCs (green) within the infarct region at the mid-infarct level from each group (scale bars: 50 μm). Nuclei were stained in blue. (B) Quantitatively, only the 250 ng group had a significantly higher density of CD31 + ECs at the infarct (p = 0.013, vs saline). (C) No significant difference in the CD31 + EC density was noted in the peri-infarct area (all p > 0.05, vs saline). (D) Only the 1,000 group had a significantly higher density of αSMA + SMCs within the infarct region (p = 0.045, vs saline). (E) No notable difference in the αSMA + SMC density in the peri-infarct area (all p > 0.05, vs saline). Note: *p < 0.05.
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    Image Search Results


    Intramyocardial injection of IL-10 enhances revascularization in the ischemic myocardium. Long-term revascularization, including angiogenesis and vasculogenesis, in the ischemic myocardium was evaluated by the presence of CD31 + endothelial cells (ECs) and αSMA + peri-vascular smooth muscle cells (SMCs), respectively, at 6 weeks post-infarction ( n = 3 per group). Perivascular SMCs defined as αSMA + cells around CD31 + ECs. Healthy (normal) hearts served as baseline controls ( n = 3). (A) Representative images of CD31 + ECs (red) and αSMA + SMCs (green) within the infarct region at the mid-infarct level from each group (scale bars: 50 μm). Nuclei were stained in blue. (B) Quantitatively, only the 250 ng group had a significantly higher density of CD31 + ECs at the infarct (p = 0.013, vs saline). (C) No significant difference in the CD31 + EC density was noted in the peri-infarct area (all p > 0.05, vs saline). (D) Only the 1,000 group had a significantly higher density of αSMA + SMCs within the infarct region (p = 0.045, vs saline). (E) No notable difference in the αSMA + SMC density in the peri-infarct area (all p > 0.05, vs saline). Note: *p < 0.05.

    Journal: Frontiers in Physiology

    Article Title: Interleukin-10 exhibit dose-dependent effects on macrophage phenotypes and cardiac remodeling after myocardial infarction

    doi: 10.3389/fphys.2024.1481460

    Figure Lengend Snippet: Intramyocardial injection of IL-10 enhances revascularization in the ischemic myocardium. Long-term revascularization, including angiogenesis and vasculogenesis, in the ischemic myocardium was evaluated by the presence of CD31 + endothelial cells (ECs) and αSMA + peri-vascular smooth muscle cells (SMCs), respectively, at 6 weeks post-infarction ( n = 3 per group). Perivascular SMCs defined as αSMA + cells around CD31 + ECs. Healthy (normal) hearts served as baseline controls ( n = 3). (A) Representative images of CD31 + ECs (red) and αSMA + SMCs (green) within the infarct region at the mid-infarct level from each group (scale bars: 50 μm). Nuclei were stained in blue. (B) Quantitatively, only the 250 ng group had a significantly higher density of CD31 + ECs at the infarct (p = 0.013, vs saline). (C) No significant difference in the CD31 + EC density was noted in the peri-infarct area (all p > 0.05, vs saline). (D) Only the 1,000 group had a significantly higher density of αSMA + SMCs within the infarct region (p = 0.045, vs saline). (E) No notable difference in the αSMA + SMC density in the peri-infarct area (all p > 0.05, vs saline). Note: *p < 0.05.

    Article Snippet: To examine vascular endothelial cells (ECs) and smooth muscle cells (SMCs), sections were first incubated overnight at 4°C with rat anti-mouse CD31 (platelet endothelial cell adhesion molecule, PECAM-1) antibody (1:100, Becton-Dickinson Biosciences, Franklin Lakes, NJ, United States), followed by donkey anti-rat-Alexa594 IgG (1:400, Life Technologies) at RT for 1 h, and subsequently incubated with mouse anti-alpha smooth muscle actin-FITC (1:100, Sigma-Aldrich).

    Techniques: Injection, Staining, Saline