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mouse brain endothelial primary cells ecs  (Celprogen Inc)


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    Celprogen Inc mouse brain endothelial primary cells ecs
    Changes in miR-155, miR-100, and miR-let-7i expression affect in <t>vitro</t> <t>endothelial</t> morphogenesis . 24 hours after transfection with specific synthetic inhibitors (A) or mimics (B), <t>ECs</t> were subjected to in vitro EC morphogenesis assay. DIC images of unlabeled cells were acquired using a Nikon TE2000 microscope and SlideBook software (DIC micrographs). GAPDH-labeled low-magnification images of the tubular structures (red, inserts) were acquired using a Zeiss LSM confocal microscope. Bars 20 μm. Graphs: Data are expressed as the average tube length, or number of branch points per visual area ± S.E.M., n = 10 wells per inhibitor/10 images per well. Student's t-test: * P < 0.05; **P < 0.01; *** P < 0.001.
    Mouse Brain Endothelial Primary Cells Ecs, supplied by Celprogen Inc, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+brain+endothelial+primary+cells+ecs/pmc03226576-36-0-9?v=Celprogen+Inc
    Average 90 stars, based on 2 article reviews
    mouse brain endothelial primary cells ecs - by Bioz Stars, 2026-08
    90/100 stars

    Images

    1) Product Images from "The role of microRNAs in neural stem cell-supported endothelial morphogenesis"

    Article Title: The role of microRNAs in neural stem cell-supported endothelial morphogenesis

    Journal: Vascular Cell

    doi: 10.1186/2045-824X-3-25

    Changes in miR-155, miR-100, and miR-let-7i expression affect in vitro endothelial morphogenesis . 24 hours after transfection with specific synthetic inhibitors (A) or mimics (B), ECs were subjected to in vitro EC morphogenesis assay. DIC images of unlabeled cells were acquired using a Nikon TE2000 microscope and SlideBook software (DIC micrographs). GAPDH-labeled low-magnification images of the tubular structures (red, inserts) were acquired using a Zeiss LSM confocal microscope. Bars 20 μm. Graphs: Data are expressed as the average tube length, or number of branch points per visual area ± S.E.M., n = 10 wells per inhibitor/10 images per well. Student's t-test: * P < 0.05; **P < 0.01; *** P < 0.001.
    Figure Legend Snippet: Changes in miR-155, miR-100, and miR-let-7i expression affect in vitro endothelial morphogenesis . 24 hours after transfection with specific synthetic inhibitors (A) or mimics (B), ECs were subjected to in vitro EC morphogenesis assay. DIC images of unlabeled cells were acquired using a Nikon TE2000 microscope and SlideBook software (DIC micrographs). GAPDH-labeled low-magnification images of the tubular structures (red, inserts) were acquired using a Zeiss LSM confocal microscope. Bars 20 μm. Graphs: Data are expressed as the average tube length, or number of branch points per visual area ± S.E.M., n = 10 wells per inhibitor/10 images per well. Student's t-test: * P < 0.05; **P < 0.01; *** P < 0.001.

    Techniques Used: Expressing, In Vitro, Transfection, Microscopy, Software, Labeling

    Hypothesis on the possible mechanisms of the pro-angiogenic effect produced by NSPCs . A: general mechanism of the NSPC-supported EC morphogenesis. NSPC-released pro-angiogenic factors induce changes in miRNA and gene expression in ECs, leading to activation of cell signaling pathways regulating EC morphogenesis and blood vessel formation. Panel B: a possible link between NSPC signaling and alterations in EC miRNA expression, leading to endothelial morphogenesis. NSPC-released pro-angiogenic factors such as VEGF, TGF-β and TNF, etc., bind to the corresponding receptors on EC surfaces, and trigger the activation of transcriptional or post-transcriptional supressors of miRNA 155, 100, and let-7i expression. Resulting downregulation (blue arrow) of miR-155, miR-100, and miR-let-7i leads to the increased (red arrow) expression of mTOR, SMAD2, and SMAD3, and thus activation of the mTOR and TGF-β signaling cascade and transcription of genes responsible for endothelial morphogenesis.
    Figure Legend Snippet: Hypothesis on the possible mechanisms of the pro-angiogenic effect produced by NSPCs . A: general mechanism of the NSPC-supported EC morphogenesis. NSPC-released pro-angiogenic factors induce changes in miRNA and gene expression in ECs, leading to activation of cell signaling pathways regulating EC morphogenesis and blood vessel formation. Panel B: a possible link between NSPC signaling and alterations in EC miRNA expression, leading to endothelial morphogenesis. NSPC-released pro-angiogenic factors such as VEGF, TGF-β and TNF, etc., bind to the corresponding receptors on EC surfaces, and trigger the activation of transcriptional or post-transcriptional supressors of miRNA 155, 100, and let-7i expression. Resulting downregulation (blue arrow) of miR-155, miR-100, and miR-let-7i leads to the increased (red arrow) expression of mTOR, SMAD2, and SMAD3, and thus activation of the mTOR and TGF-β signaling cascade and transcription of genes responsible for endothelial morphogenesis.

    Techniques Used: Produced, Expressing, Activation Assay



    Similar Products

    mouse brain endothelial primary cells ecs  (Celprogen Inc)
    90
    Celprogen Inc mouse brain endothelial primary cells ecs
    Changes in miR-155, miR-100, and miR-let-7i expression affect in <t>vitro</t> <t>endothelial</t> morphogenesis . 24 hours after transfection with specific synthetic inhibitors (A) or mimics (B), <t>ECs</t> were subjected to in vitro EC morphogenesis assay. DIC images of unlabeled cells were acquired using a Nikon TE2000 microscope and SlideBook software (DIC micrographs). GAPDH-labeled low-magnification images of the tubular structures (red, inserts) were acquired using a Zeiss LSM confocal microscope. Bars 20 μm. Graphs: Data are expressed as the average tube length, or number of branch points per visual area ± S.E.M., n = 10 wells per inhibitor/10 images per well. Student's t-test: * P < 0.05; **P < 0.01; *** P < 0.001.
    Mouse Brain Endothelial Primary Cells Ecs, supplied by Celprogen 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/mouse+brain+endothelial+primary+cells+ecs/pmc03226576-36-0-9?v=Celprogen+Inc
    Average 90 stars, based on 1 article reviews
    mouse brain endothelial primary cells ecs - by Bioz Stars, 2026-08
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    Changes in miR-155, miR-100, and miR-let-7i expression affect in vitro endothelial morphogenesis . 24 hours after transfection with specific synthetic inhibitors (A) or mimics (B), ECs were subjected to in vitro EC morphogenesis assay. DIC images of unlabeled cells were acquired using a Nikon TE2000 microscope and SlideBook software (DIC micrographs). GAPDH-labeled low-magnification images of the tubular structures (red, inserts) were acquired using a Zeiss LSM confocal microscope. Bars 20 μm. Graphs: Data are expressed as the average tube length, or number of branch points per visual area ± S.E.M., n = 10 wells per inhibitor/10 images per well. Student's t-test: * P < 0.05; **P < 0.01; *** P < 0.001.

    Journal: Vascular Cell

    Article Title: The role of microRNAs in neural stem cell-supported endothelial morphogenesis

    doi: 10.1186/2045-824X-3-25

    Figure Lengend Snippet: Changes in miR-155, miR-100, and miR-let-7i expression affect in vitro endothelial morphogenesis . 24 hours after transfection with specific synthetic inhibitors (A) or mimics (B), ECs were subjected to in vitro EC morphogenesis assay. DIC images of unlabeled cells were acquired using a Nikon TE2000 microscope and SlideBook software (DIC micrographs). GAPDH-labeled low-magnification images of the tubular structures (red, inserts) were acquired using a Zeiss LSM confocal microscope. Bars 20 μm. Graphs: Data are expressed as the average tube length, or number of branch points per visual area ± S.E.M., n = 10 wells per inhibitor/10 images per well. Student's t-test: * P < 0.05; **P < 0.01; *** P < 0.001.

    Article Snippet: Mouse brain endothelial primary cells (ECs) were purchased from Celprogen (San Diego, CA).

    Techniques: Expressing, In Vitro, Transfection, Microscopy, Software, Labeling

    Hypothesis on the possible mechanisms of the pro-angiogenic effect produced by NSPCs . A: general mechanism of the NSPC-supported EC morphogenesis. NSPC-released pro-angiogenic factors induce changes in miRNA and gene expression in ECs, leading to activation of cell signaling pathways regulating EC morphogenesis and blood vessel formation. Panel B: a possible link between NSPC signaling and alterations in EC miRNA expression, leading to endothelial morphogenesis. NSPC-released pro-angiogenic factors such as VEGF, TGF-β and TNF, etc., bind to the corresponding receptors on EC surfaces, and trigger the activation of transcriptional or post-transcriptional supressors of miRNA 155, 100, and let-7i expression. Resulting downregulation (blue arrow) of miR-155, miR-100, and miR-let-7i leads to the increased (red arrow) expression of mTOR, SMAD2, and SMAD3, and thus activation of the mTOR and TGF-β signaling cascade and transcription of genes responsible for endothelial morphogenesis.

    Journal: Vascular Cell

    Article Title: The role of microRNAs in neural stem cell-supported endothelial morphogenesis

    doi: 10.1186/2045-824X-3-25

    Figure Lengend Snippet: Hypothesis on the possible mechanisms of the pro-angiogenic effect produced by NSPCs . A: general mechanism of the NSPC-supported EC morphogenesis. NSPC-released pro-angiogenic factors induce changes in miRNA and gene expression in ECs, leading to activation of cell signaling pathways regulating EC morphogenesis and blood vessel formation. Panel B: a possible link between NSPC signaling and alterations in EC miRNA expression, leading to endothelial morphogenesis. NSPC-released pro-angiogenic factors such as VEGF, TGF-β and TNF, etc., bind to the corresponding receptors on EC surfaces, and trigger the activation of transcriptional or post-transcriptional supressors of miRNA 155, 100, and let-7i expression. Resulting downregulation (blue arrow) of miR-155, miR-100, and miR-let-7i leads to the increased (red arrow) expression of mTOR, SMAD2, and SMAD3, and thus activation of the mTOR and TGF-β signaling cascade and transcription of genes responsible for endothelial morphogenesis.

    Article Snippet: Mouse brain endothelial primary cells (ECs) were purchased from Celprogen (San Diego, CA).

    Techniques: Produced, Expressing, Activation Assay