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oe exosomes  (Exosome Diagnostics)

 
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    Exosome Diagnostics oe exosomes
    The regulatory mchanisms of miR-96-5p in AF biology. (A) Time-course analysis of miR-96–5p expression in AFs treated with PVPAC-Exo at 0, 6, 12, and 24 h. (B) and (C) AFs were transfected with miR-96–5p mimic and NC mimic for 24 h. Then, the migration ability of AFs through migration experiments (B) and EDU assay (C) were evaluated using Image J and GraphPad Prism 9. vs. control mimic, ∗P < 0.05, ∗∗P < 0.01, n (the number of experiments) = 3, scale bar = 150 μm. (D) Correlation analysis between extracellular ncRNA levels in culture supernatant and intracellular expression of PHF20L1 and MEOX2 by RT-qPCR. (E) Bioinformatic prediction identifying PHF20L1 and MEOX2 as potential targets of miR-96–5p. (F) Predicted miR-96–5p binding sites in the 3′UTR of PHF20L1. (G) Luciferase reporter assay displayed that miR-96–5p mimic significantly reduced luciferase activity in the PHF20L1-WT group, but not in the PHF20L1-Mut group (vs. PHF20L1-Mut, ∗∗ P < 0.01), n (the number of experiments) = 3. (H) Bioinformatics analysis indicated the miR-96–5p binding sites in the 3′UTR of MEOX2. (I) Western blot exhibited no significant change in MEOX2 protein levels upon miR-96–5p overexpression. (J) Interaction network among miR-96–5p, circEif3c, PHF20L1, and MEOX2, constructed using GEPIA, ENCORI, miRNet, NDEx, and Cytoscape. (K) Western blot analysis of PHF20L1 and MEOX2 expression in AFs transfected with control-exosome, <t>OE-exosomes,</t> miR-comtrol mimic, miR-96–5p mimic, and UNC1215, respectively. vs. control-exosome, miR-comtrol mimic, ∗ P < 0.05, ∗∗ P < 0.01, n (the number of experiments) = 3. (L) Predicted protein–protein interaction interface between PHF20L1 and MEOX2 using Zdock 3.0.2 and PyMOL 2.5.5. (M) Co-IP experiments confirmed an interaction between PHF20L1 and MEOX2.
    Oe Exosomes, supplied by Exosome Diagnostics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "CircEif3c/miR-96–5p/PHF20L1/MEOX2 axis in perivascular preadipocyte exosomes mediates fibroblast dysfunction and vascular remodeling"

    Article Title: CircEif3c/miR-96–5p/PHF20L1/MEOX2 axis in perivascular preadipocyte exosomes mediates fibroblast dysfunction and vascular remodeling

    Journal: Non-coding RNA Research

    doi: 10.1016/j.ncrna.2026.01.006

    The regulatory mchanisms of miR-96-5p in AF biology. (A) Time-course analysis of miR-96–5p expression in AFs treated with PVPAC-Exo at 0, 6, 12, and 24 h. (B) and (C) AFs were transfected with miR-96–5p mimic and NC mimic for 24 h. Then, the migration ability of AFs through migration experiments (B) and EDU assay (C) were evaluated using Image J and GraphPad Prism 9. vs. control mimic, ∗P < 0.05, ∗∗P < 0.01, n (the number of experiments) = 3, scale bar = 150 μm. (D) Correlation analysis between extracellular ncRNA levels in culture supernatant and intracellular expression of PHF20L1 and MEOX2 by RT-qPCR. (E) Bioinformatic prediction identifying PHF20L1 and MEOX2 as potential targets of miR-96–5p. (F) Predicted miR-96–5p binding sites in the 3′UTR of PHF20L1. (G) Luciferase reporter assay displayed that miR-96–5p mimic significantly reduced luciferase activity in the PHF20L1-WT group, but not in the PHF20L1-Mut group (vs. PHF20L1-Mut, ∗∗ P < 0.01), n (the number of experiments) = 3. (H) Bioinformatics analysis indicated the miR-96–5p binding sites in the 3′UTR of MEOX2. (I) Western blot exhibited no significant change in MEOX2 protein levels upon miR-96–5p overexpression. (J) Interaction network among miR-96–5p, circEif3c, PHF20L1, and MEOX2, constructed using GEPIA, ENCORI, miRNet, NDEx, and Cytoscape. (K) Western blot analysis of PHF20L1 and MEOX2 expression in AFs transfected with control-exosome, OE-exosomes, miR-comtrol mimic, miR-96–5p mimic, and UNC1215, respectively. vs. control-exosome, miR-comtrol mimic, ∗ P < 0.05, ∗∗ P < 0.01, n (the number of experiments) = 3. (L) Predicted protein–protein interaction interface between PHF20L1 and MEOX2 using Zdock 3.0.2 and PyMOL 2.5.5. (M) Co-IP experiments confirmed an interaction between PHF20L1 and MEOX2.
    Figure Legend Snippet: The regulatory mchanisms of miR-96-5p in AF biology. (A) Time-course analysis of miR-96–5p expression in AFs treated with PVPAC-Exo at 0, 6, 12, and 24 h. (B) and (C) AFs were transfected with miR-96–5p mimic and NC mimic for 24 h. Then, the migration ability of AFs through migration experiments (B) and EDU assay (C) were evaluated using Image J and GraphPad Prism 9. vs. control mimic, ∗P < 0.05, ∗∗P < 0.01, n (the number of experiments) = 3, scale bar = 150 μm. (D) Correlation analysis between extracellular ncRNA levels in culture supernatant and intracellular expression of PHF20L1 and MEOX2 by RT-qPCR. (E) Bioinformatic prediction identifying PHF20L1 and MEOX2 as potential targets of miR-96–5p. (F) Predicted miR-96–5p binding sites in the 3′UTR of PHF20L1. (G) Luciferase reporter assay displayed that miR-96–5p mimic significantly reduced luciferase activity in the PHF20L1-WT group, but not in the PHF20L1-Mut group (vs. PHF20L1-Mut, ∗∗ P < 0.01), n (the number of experiments) = 3. (H) Bioinformatics analysis indicated the miR-96–5p binding sites in the 3′UTR of MEOX2. (I) Western blot exhibited no significant change in MEOX2 protein levels upon miR-96–5p overexpression. (J) Interaction network among miR-96–5p, circEif3c, PHF20L1, and MEOX2, constructed using GEPIA, ENCORI, miRNet, NDEx, and Cytoscape. (K) Western blot analysis of PHF20L1 and MEOX2 expression in AFs transfected with control-exosome, OE-exosomes, miR-comtrol mimic, miR-96–5p mimic, and UNC1215, respectively. vs. control-exosome, miR-comtrol mimic, ∗ P < 0.05, ∗∗ P < 0.01, n (the number of experiments) = 3. (L) Predicted protein–protein interaction interface between PHF20L1 and MEOX2 using Zdock 3.0.2 and PyMOL 2.5.5. (M) Co-IP experiments confirmed an interaction between PHF20L1 and MEOX2.

    Techniques Used: Expressing, Transfection, Migration, EdU Assay, Control, Quantitative RT-PCR, Binding Assay, Luciferase, Reporter Assay, Activity Assay, Western Blot, Over Expression, Construct, Co-Immunoprecipitation Assay



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    The regulatory mchanisms of miR-96-5p in AF biology. (A) Time-course analysis of miR-96–5p expression in AFs treated with PVPAC-Exo at 0, 6, 12, and 24 h. (B) and (C) AFs were transfected with miR-96–5p mimic and NC mimic for 24 h. Then, the migration ability of AFs through migration experiments (B) and EDU assay (C) were evaluated using Image J and GraphPad Prism 9. vs. control mimic, ∗P < 0.05, ∗∗P < 0.01, n (the number of experiments) = 3, scale bar = 150 μm. (D) Correlation analysis between extracellular ncRNA levels in culture supernatant and intracellular expression of PHF20L1 and MEOX2 by RT-qPCR. (E) Bioinformatic prediction identifying PHF20L1 and MEOX2 as potential targets of miR-96–5p. (F) Predicted miR-96–5p binding sites in the 3′UTR of PHF20L1. (G) Luciferase reporter assay displayed that miR-96–5p mimic significantly reduced luciferase activity in the PHF20L1-WT group, but not in the PHF20L1-Mut group (vs. PHF20L1-Mut, ∗∗ P < 0.01), n (the number of experiments) = 3. (H) Bioinformatics analysis indicated the miR-96–5p binding sites in the 3′UTR of MEOX2. (I) Western blot exhibited no significant change in MEOX2 protein levels upon miR-96–5p overexpression. (J) Interaction network among miR-96–5p, circEif3c, PHF20L1, and MEOX2, constructed using GEPIA, ENCORI, miRNet, NDEx, and Cytoscape. (K) Western blot analysis of PHF20L1 and MEOX2 expression in AFs transfected with control-exosome, <t>OE-exosomes,</t> miR-comtrol mimic, miR-96–5p mimic, and UNC1215, respectively. vs. control-exosome, miR-comtrol mimic, ∗ P < 0.05, ∗∗ P < 0.01, n (the number of experiments) = 3. (L) Predicted protein–protein interaction interface between PHF20L1 and MEOX2 using Zdock 3.0.2 and PyMOL 2.5.5. (M) Co-IP experiments confirmed an interaction between PHF20L1 and MEOX2.
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    The regulatory mchanisms of miR-96-5p in AF biology. (A) Time-course analysis of miR-96–5p expression in AFs treated with PVPAC-Exo at 0, 6, 12, and 24 h. (B) and (C) AFs were transfected with miR-96–5p mimic and NC mimic for 24 h. Then, the migration ability of AFs through migration experiments (B) and EDU assay (C) were evaluated using Image J and GraphPad Prism 9. vs. control mimic, ∗P < 0.05, ∗∗P < 0.01, n (the number of experiments) = 3, scale bar = 150 μm. (D) Correlation analysis between extracellular ncRNA levels in culture supernatant and intracellular expression of PHF20L1 and MEOX2 by RT-qPCR. (E) Bioinformatic prediction identifying PHF20L1 and MEOX2 as potential targets of miR-96–5p. (F) Predicted miR-96–5p binding sites in the 3′UTR of PHF20L1. (G) Luciferase reporter assay displayed that miR-96–5p mimic significantly reduced luciferase activity in the PHF20L1-WT group, but not in the PHF20L1-Mut group (vs. PHF20L1-Mut, ∗∗ P < 0.01), n (the number of experiments) = 3. (H) Bioinformatics analysis indicated the miR-96–5p binding sites in the 3′UTR of MEOX2. (I) Western blot exhibited no significant change in MEOX2 protein levels upon miR-96–5p overexpression. (J) Interaction network among miR-96–5p, circEif3c, PHF20L1, and MEOX2, constructed using GEPIA, ENCORI, miRNet, NDEx, and Cytoscape. (K) Western blot analysis of PHF20L1 and MEOX2 expression in AFs transfected with control-exosome, <t>OE-exosomes,</t> miR-comtrol mimic, miR-96–5p mimic, and UNC1215, respectively. vs. control-exosome, miR-comtrol mimic, ∗ P < 0.05, ∗∗ P < 0.01, n (the number of experiments) = 3. (L) Predicted protein–protein interaction interface between PHF20L1 and MEOX2 using Zdock 3.0.2 and PyMOL 2.5.5. (M) Co-IP experiments confirmed an interaction between PHF20L1 and MEOX2.
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    The regulatory mchanisms of miR-96-5p in AF biology. (A) Time-course analysis of miR-96–5p expression in AFs treated with PVPAC-Exo at 0, 6, 12, and 24 h. (B) and (C) AFs were transfected with miR-96–5p mimic and NC mimic for 24 h. Then, the migration ability of AFs through migration experiments (B) and EDU assay (C) were evaluated using Image J and GraphPad Prism 9. vs. control mimic, ∗P < 0.05, ∗∗P < 0.01, n (the number of experiments) = 3, scale bar = 150 μm. (D) Correlation analysis between extracellular ncRNA levels in culture supernatant and intracellular expression of PHF20L1 and MEOX2 by RT-qPCR. (E) Bioinformatic prediction identifying PHF20L1 and MEOX2 as potential targets of miR-96–5p. (F) Predicted miR-96–5p binding sites in the 3′UTR of PHF20L1. (G) Luciferase reporter assay displayed that miR-96–5p mimic significantly reduced luciferase activity in the PHF20L1-WT group, but not in the PHF20L1-Mut group (vs. PHF20L1-Mut, ∗∗ P < 0.01), n (the number of experiments) = 3. (H) Bioinformatics analysis indicated the miR-96–5p binding sites in the 3′UTR of MEOX2. (I) Western blot exhibited no significant change in MEOX2 protein levels upon miR-96–5p overexpression. (J) Interaction network among miR-96–5p, circEif3c, PHF20L1, and MEOX2, constructed using GEPIA, ENCORI, miRNet, NDEx, and Cytoscape. (K) Western blot analysis of PHF20L1 and MEOX2 expression in AFs transfected with control-exosome, <t>OE-exosomes,</t> miR-comtrol mimic, miR-96–5p mimic, and UNC1215, respectively. vs. control-exosome, miR-comtrol mimic, ∗ P < 0.05, ∗∗ P < 0.01, n (the number of experiments) = 3. (L) Predicted protein–protein interaction interface between PHF20L1 and MEOX2 using Zdock 3.0.2 and PyMOL 2.5.5. (M) Co-IP experiments confirmed an interaction between PHF20L1 and MEOX2.
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    The regulatory mchanisms of miR-96-5p in AF biology. (A) Time-course analysis of miR-96–5p expression in AFs treated with PVPAC-Exo at 0, 6, 12, and 24 h. (B) and (C) AFs were transfected with miR-96–5p mimic and NC mimic for 24 h. Then, the migration ability of AFs through migration experiments (B) and EDU assay (C) were evaluated using Image J and GraphPad Prism 9. vs. control mimic, ∗P < 0.05, ∗∗P < 0.01, n (the number of experiments) = 3, scale bar = 150 μm. (D) Correlation analysis between extracellular ncRNA levels in culture supernatant and intracellular expression of PHF20L1 and MEOX2 by RT-qPCR. (E) Bioinformatic prediction identifying PHF20L1 and MEOX2 as potential targets of miR-96–5p. (F) Predicted miR-96–5p binding sites in the 3′UTR of PHF20L1. (G) Luciferase reporter assay displayed that miR-96–5p mimic significantly reduced luciferase activity in the PHF20L1-WT group, but not in the PHF20L1-Mut group (vs. PHF20L1-Mut, ∗∗ P < 0.01), n (the number of experiments) = 3. (H) Bioinformatics analysis indicated the miR-96–5p binding sites in the 3′UTR of MEOX2. (I) Western blot exhibited no significant change in MEOX2 protein levels upon miR-96–5p overexpression. (J) Interaction network among miR-96–5p, circEif3c, PHF20L1, and MEOX2, constructed using GEPIA, ENCORI, miRNet, NDEx, and Cytoscape. (K) Western blot analysis of PHF20L1 and MEOX2 expression in AFs transfected with control-exosome, <t>OE-exosomes,</t> miR-comtrol mimic, miR-96–5p mimic, and UNC1215, respectively. vs. control-exosome, miR-comtrol mimic, ∗ P < 0.05, ∗∗ P < 0.01, n (the number of experiments) = 3. (L) Predicted protein–protein interaction interface between PHF20L1 and MEOX2 using Zdock 3.0.2 and PyMOL 2.5.5. (M) Co-IP experiments confirmed an interaction between PHF20L1 and MEOX2.
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    The regulatory mchanisms of miR-96-5p in AF biology. (A) Time-course analysis of miR-96–5p expression in AFs treated with PVPAC-Exo at 0, 6, 12, and 24 h. (B) and (C) AFs were transfected with miR-96–5p mimic and NC mimic for 24 h. Then, the migration ability of AFs through migration experiments (B) and EDU assay (C) were evaluated using Image J and GraphPad Prism 9. vs. control mimic, ∗P < 0.05, ∗∗P < 0.01, n (the number of experiments) = 3, scale bar = 150 μm. (D) Correlation analysis between extracellular ncRNA levels in culture supernatant and intracellular expression of PHF20L1 and MEOX2 by RT-qPCR. (E) Bioinformatic prediction identifying PHF20L1 and MEOX2 as potential targets of miR-96–5p. (F) Predicted miR-96–5p binding sites in the 3′UTR of PHF20L1. (G) Luciferase reporter assay displayed that miR-96–5p mimic significantly reduced luciferase activity in the PHF20L1-WT group, but not in the PHF20L1-Mut group (vs. PHF20L1-Mut, ∗∗ P < 0.01), n (the number of experiments) = 3. (H) Bioinformatics analysis indicated the miR-96–5p binding sites in the 3′UTR of MEOX2. (I) Western blot exhibited no significant change in MEOX2 protein levels upon miR-96–5p overexpression. (J) Interaction network among miR-96–5p, circEif3c, PHF20L1, and MEOX2, constructed using GEPIA, ENCORI, miRNet, NDEx, and Cytoscape. (K) Western blot analysis of PHF20L1 and MEOX2 expression in AFs transfected with control-exosome, OE-exosomes, miR-comtrol mimic, miR-96–5p mimic, and UNC1215, respectively. vs. control-exosome, miR-comtrol mimic, ∗ P < 0.05, ∗∗ P < 0.01, n (the number of experiments) = 3. (L) Predicted protein–protein interaction interface between PHF20L1 and MEOX2 using Zdock 3.0.2 and PyMOL 2.5.5. (M) Co-IP experiments confirmed an interaction between PHF20L1 and MEOX2.

    Journal: Non-coding RNA Research

    Article Title: CircEif3c/miR-96–5p/PHF20L1/MEOX2 axis in perivascular preadipocyte exosomes mediates fibroblast dysfunction and vascular remodeling

    doi: 10.1016/j.ncrna.2026.01.006

    Figure Lengend Snippet: The regulatory mchanisms of miR-96-5p in AF biology. (A) Time-course analysis of miR-96–5p expression in AFs treated with PVPAC-Exo at 0, 6, 12, and 24 h. (B) and (C) AFs were transfected with miR-96–5p mimic and NC mimic for 24 h. Then, the migration ability of AFs through migration experiments (B) and EDU assay (C) were evaluated using Image J and GraphPad Prism 9. vs. control mimic, ∗P < 0.05, ∗∗P < 0.01, n (the number of experiments) = 3, scale bar = 150 μm. (D) Correlation analysis between extracellular ncRNA levels in culture supernatant and intracellular expression of PHF20L1 and MEOX2 by RT-qPCR. (E) Bioinformatic prediction identifying PHF20L1 and MEOX2 as potential targets of miR-96–5p. (F) Predicted miR-96–5p binding sites in the 3′UTR of PHF20L1. (G) Luciferase reporter assay displayed that miR-96–5p mimic significantly reduced luciferase activity in the PHF20L1-WT group, but not in the PHF20L1-Mut group (vs. PHF20L1-Mut, ∗∗ P < 0.01), n (the number of experiments) = 3. (H) Bioinformatics analysis indicated the miR-96–5p binding sites in the 3′UTR of MEOX2. (I) Western blot exhibited no significant change in MEOX2 protein levels upon miR-96–5p overexpression. (J) Interaction network among miR-96–5p, circEif3c, PHF20L1, and MEOX2, constructed using GEPIA, ENCORI, miRNet, NDEx, and Cytoscape. (K) Western blot analysis of PHF20L1 and MEOX2 expression in AFs transfected with control-exosome, OE-exosomes, miR-comtrol mimic, miR-96–5p mimic, and UNC1215, respectively. vs. control-exosome, miR-comtrol mimic, ∗ P < 0.05, ∗∗ P < 0.01, n (the number of experiments) = 3. (L) Predicted protein–protein interaction interface between PHF20L1 and MEOX2 using Zdock 3.0.2 and PyMOL 2.5.5. (M) Co-IP experiments confirmed an interaction between PHF20L1 and MEOX2.

    Article Snippet: OE-exosomes significantly increased the expression of vimentin and PHF20L1 while decreasing MEOX2 levels compared to controls (control-exosome or miR-control).

    Techniques: Expressing, Transfection, Migration, EdU Assay, Control, Quantitative RT-PCR, Binding Assay, Luciferase, Reporter Assay, Activity Assay, Western Blot, Over Expression, Construct, Co-Immunoprecipitation Assay