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e click edu cell proliferation imaging assay kit  (Elabscience Biotechnology)


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    Elabscience Biotechnology e click edu cell proliferation imaging assay kit
    E Click Edu Cell Proliferation Imaging Assay Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 59 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/e click edu cell proliferation imaging assay kit/product/Elabscience Biotechnology
    Average 95 stars, based on 59 article reviews
    e click edu cell proliferation imaging assay kit - by Bioz Stars, 2026-05
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    Profibrotic macrophages increasing fibroblast <t>proliferation</t> via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).
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    Profibrotic macrophages increasing fibroblast <t>proliferation</t> via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).
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    Profibrotic macrophages increasing fibroblast <t>proliferation</t> via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).
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    Profibrotic macrophages increasing fibroblast <t>proliferation</t> via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).
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    Profibrotic macrophages increasing fibroblast <t>proliferation</t> via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).
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    Profibrotic macrophages increasing fibroblast <t>proliferation</t> via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).
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    Profibrotic macrophages increasing fibroblast <t>proliferation</t> via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).
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    Profibrotic macrophages increasing fibroblast <t>proliferation</t> via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).
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    Profibrotic macrophages increasing fibroblast <t>proliferation</t> via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).
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    MiR15a/16 suppress cellular growth and protein anabolism in NSCLC. Overexpression of miR15a/16 in LUSC (H446) and LUAD (A549) cells slows cellular <t>proliferation</t> over 72 h (panel A, B) and blunts protein synthesis rates (panel C, D) in models of NSCLC. For proliferation experiments (panels A, B) n = 5, for protein synthesis measurements n = 4. * indicates a difference of p < 0.05, **** indicates a difference of p < 0.0001.
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    Image Search Results


    Profibrotic macrophages increasing fibroblast proliferation via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).

    Journal: Bioactive Materials

    Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

    doi: 10.1016/j.bioactmat.2026.01.029

    Figure Lengend Snippet: Profibrotic macrophages increasing fibroblast proliferation via their secreted IGF-1. (a) Dot plots of Igf1 expression in C2 and the other subgroups of macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. (b) Igf1 expression score in macrophages in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (c) Quantification of IGF-1 concentration in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). UMAP of fibroblasts in regenerated aortas 30 days (d) and 90 days (e) after graft implantation in WT and Apoe −/− rats, heatmap of cell cycle (Ccnd1, Ccnd2, and Ccnd3) scores in UMAP of fibroblasts, and box plots of cell cycle scores in fibroblasts. ∗∗∗∗ indicates p < 0.0001, unpaired t -test. (f) Immunofluorescence staining of Ki67 in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe −/− rats. L indicates lumens. (g) Quantification of Ki67 positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different animals were analyzed (n = 5). (h) Quantification of IGF-1 in culture mediums of WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h by ELISA. ∗∗ indicates p < 0.01, unpaired t -test. For each group, three different samples were analyzed (n = 3). (i) Immunofluorescence staining of Ki67 in WT and APOE KO fibroblasts after treatment with IGF-1 (10 ng/mL) for 24 h. Cells were counterstained with phalloidin. (j) Quantification of proliferation of WT and APOE KO fibroblasts treated with IGF-1 (10 ng/mL) for 24 h using cell counting kit-8 (CCK-8). ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (k) Quantification of proliferation of WT fibroblasts treated with conditioned medium (CM) with or without IGF-1 blocking antibody (Ab, 1 μg/mL) for 24 h using CCK-8. CM were medium conditioned by WT macrophages cultured on PCL scaffolds for 48 h ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3).

    Article Snippet: Cell proliferation was assayed using cell counting kit-8 (CCK-8, Dojindo) as manuals.

    Techniques: Expressing, Concentration Assay, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Cell Counting, CCK-8 Assay, Blocking Assay, Cell Culture

    MiR15a/16 suppress cellular growth and protein anabolism in NSCLC. Overexpression of miR15a/16 in LUSC (H446) and LUAD (A549) cells slows cellular proliferation over 72 h (panel A, B) and blunts protein synthesis rates (panel C, D) in models of NSCLC. For proliferation experiments (panels A, B) n = 5, for protein synthesis measurements n = 4. * indicates a difference of p < 0.05, **** indicates a difference of p < 0.0001.

    Journal: FASEB BioAdvances

    Article Title: MicroRNA 15a and 16 Regulate Proteostasis in Non‐Small Cell Lung Cancer

    doi: 10.1096/fba.2026-00075

    Figure Lengend Snippet: MiR15a/16 suppress cellular growth and protein anabolism in NSCLC. Overexpression of miR15a/16 in LUSC (H446) and LUAD (A549) cells slows cellular proliferation over 72 h (panel A, B) and blunts protein synthesis rates (panel C, D) in models of NSCLC. For proliferation experiments (panels A, B) n = 5, for protein synthesis measurements n = 4. * indicates a difference of p < 0.05, **** indicates a difference of p < 0.0001.

    Article Snippet: We measured cellular proliferation using a WST‐8 assay (HY‐K0301; MedChemExpress, Monmouth Junction, NJ, USA), a colorimetric assay that produces a tetrazolium salt in proportion to the number of cells in a sample well.

    Techniques: Over Expression