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primary human vascular umbilical vein endothelial cells  (Cell Applications Inc)


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    Cell Applications Inc primary human vascular umbilical vein endothelial cells
    Primary Human Vascular Umbilical Vein Endothelial Cells, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 95/100, based on 274 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary human vascular umbilical vein endothelial cells/product/Cell Applications Inc
    Average 95 stars, based on 274 article reviews
    primary human vascular umbilical vein endothelial cells - by Bioz Stars, 2026-02
    95/100 stars

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    ATCC normal primary human vascular endothelial cells huvec
    rhMG53 inhibits vascular <t>endothelial</t> cell migration and tube formation. ( A ) rhMG53 did not induce cellular toxicity in <t>HUVEC</t> up to 100 μg/mL ( n = 5; ** p = 0.01). ( B ) Representative photomicrographs 24 h after scratch wounding, HUVEC treated with 50 μg/mL rhMG53 had significantly less migration and proliferation compared to control ( n = 9). Magnification 4×. ( C ) Quantification of the scratch area remaining at 24 h (**** p < 0.0001). ( D ) Representative photomicrographs and quantification of tube formation when HUVEC was seeded on Matrigel, followed by treatment with VEGF (10 ng/mL) with or without rhMG53 (50 μg/mL) for 18 h. rhMG53 significantly reduced tube length in VEGF-treated HUVEC ( n = 4; ** p = 0.0029). Magnification 4×. ( E ) HUVEC treated with IL-1B (10 ng/mL) with or without rhMG53 have decreased pSTAT3 protein expression; when normalized to total STAT3 expression, rhMG53 significantly (** p = 0.0084) decreased pSTAT3 ( n = 4). Statistical significance was assessed with the Kruskal–Wallis nonparametric test.
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    rhMG53 inhibits vascular <t>endothelial</t> cell migration and tube formation. ( A ) rhMG53 did not induce cellular toxicity in <t>HUVEC</t> up to 100 μg/mL ( n = 5; ** p = 0.01). ( B ) Representative photomicrographs 24 h after scratch wounding, HUVEC treated with 50 μg/mL rhMG53 had significantly less migration and proliferation compared to control ( n = 9). Magnification 4×. ( C ) Quantification of the scratch area remaining at 24 h (**** p < 0.0001). ( D ) Representative photomicrographs and quantification of tube formation when HUVEC was seeded on Matrigel, followed by treatment with VEGF (10 ng/mL) with or without rhMG53 (50 μg/mL) for 18 h. rhMG53 significantly reduced tube length in VEGF-treated HUVEC ( n = 4; ** p = 0.0029). Magnification 4×. ( E ) HUVEC treated with IL-1B (10 ng/mL) with or without rhMG53 have decreased pSTAT3 protein expression; when normalized to total STAT3 expression, rhMG53 significantly (** p = 0.0084) decreased pSTAT3 ( n = 4). Statistical significance was assessed with the Kruskal–Wallis nonparametric test.
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    ATCC human vascular endothelial cell
    Role of SNHG12 in vascular <t>endothelial</t> cell function. (a) SNHG12 levels in different HUVECs groups based on RT‐qPCR results. (b) Cell viability of HUVECs based on CCK‐8 assay. (c) Cell migration of HUVECs based on cell transwell assay. (d) Cell apoptosis of HUVECs based on flow cytometry assay. (e) Concentration of inflammatory cytokines including TNF‐α, IL‐6, and IL‐1β in the culture supernatant of HUVECs based on ELISA results. (f) Concentration of adhesion factors, namely SELP, VCAM‐1 and ICAM‐1 in the culture supernatant of HUVECs based on ELISA results. ** p < 0.01, *** p < 0.001.
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    rhMG53 inhibits vascular endothelial cell migration and tube formation. ( A ) rhMG53 did not induce cellular toxicity in HUVEC up to 100 μg/mL ( n = 5; ** p = 0.01). ( B ) Representative photomicrographs 24 h after scratch wounding, HUVEC treated with 50 μg/mL rhMG53 had significantly less migration and proliferation compared to control ( n = 9). Magnification 4×. ( C ) Quantification of the scratch area remaining at 24 h (**** p < 0.0001). ( D ) Representative photomicrographs and quantification of tube formation when HUVEC was seeded on Matrigel, followed by treatment with VEGF (10 ng/mL) with or without rhMG53 (50 μg/mL) for 18 h. rhMG53 significantly reduced tube length in VEGF-treated HUVEC ( n = 4; ** p = 0.0029). Magnification 4×. ( E ) HUVEC treated with IL-1B (10 ng/mL) with or without rhMG53 have decreased pSTAT3 protein expression; when normalized to total STAT3 expression, rhMG53 significantly (** p = 0.0084) decreased pSTAT3 ( n = 4). Statistical significance was assessed with the Kruskal–Wallis nonparametric test.

    Journal: Pharmaceutics

    Article Title: Development of an Ophthalmic Hydrogel to Deliver MG53 and Promote Corneal Wound Healing

    doi: 10.3390/pharmaceutics17040526

    Figure Lengend Snippet: rhMG53 inhibits vascular endothelial cell migration and tube formation. ( A ) rhMG53 did not induce cellular toxicity in HUVEC up to 100 μg/mL ( n = 5; ** p = 0.01). ( B ) Representative photomicrographs 24 h after scratch wounding, HUVEC treated with 50 μg/mL rhMG53 had significantly less migration and proliferation compared to control ( n = 9). Magnification 4×. ( C ) Quantification of the scratch area remaining at 24 h (**** p < 0.0001). ( D ) Representative photomicrographs and quantification of tube formation when HUVEC was seeded on Matrigel, followed by treatment with VEGF (10 ng/mL) with or without rhMG53 (50 μg/mL) for 18 h. rhMG53 significantly reduced tube length in VEGF-treated HUVEC ( n = 4; ** p = 0.0029). Magnification 4×. ( E ) HUVEC treated with IL-1B (10 ng/mL) with or without rhMG53 have decreased pSTAT3 protein expression; when normalized to total STAT3 expression, rhMG53 significantly (** p = 0.0084) decreased pSTAT3 ( n = 4). Statistical significance was assessed with the Kruskal–Wallis nonparametric test.

    Article Snippet: Normal primary human vascular endothelial cells (HUVEC) were purchased from ATCC (Manassas, VA, USA) and grown in F-12K medium containing endothelial cell growth supplement.

    Techniques: Migration, Control, Expressing

    Role of SNHG12 in vascular endothelial cell function. (a) SNHG12 levels in different HUVECs groups based on RT‐qPCR results. (b) Cell viability of HUVECs based on CCK‐8 assay. (c) Cell migration of HUVECs based on cell transwell assay. (d) Cell apoptosis of HUVECs based on flow cytometry assay. (e) Concentration of inflammatory cytokines including TNF‐α, IL‐6, and IL‐1β in the culture supernatant of HUVECs based on ELISA results. (f) Concentration of adhesion factors, namely SELP, VCAM‐1 and ICAM‐1 in the culture supernatant of HUVECs based on ELISA results. ** p < 0.01, *** p < 0.001.

    Journal: Clinical and Translational Science

    Article Title: Clinical significance and underlying mechanism of long non‐coding RNA SNHG12 in lower extremity deep venous thrombosis

    doi: 10.1111/cts.70023

    Figure Lengend Snippet: Role of SNHG12 in vascular endothelial cell function. (a) SNHG12 levels in different HUVECs groups based on RT‐qPCR results. (b) Cell viability of HUVECs based on CCK‐8 assay. (c) Cell migration of HUVECs based on cell transwell assay. (d) Cell apoptosis of HUVECs based on flow cytometry assay. (e) Concentration of inflammatory cytokines including TNF‐α, IL‐6, and IL‐1β in the culture supernatant of HUVECs based on ELISA results. (f) Concentration of adhesion factors, namely SELP, VCAM‐1 and ICAM‐1 in the culture supernatant of HUVECs based on ELISA results. ** p < 0.01, *** p < 0.001.

    Article Snippet: Human vascular endothelial cell (HUVEC; catalog number: PCS‐100‐010) was gained from American Type Culture Collection (ATCC) and maintained in Dulbecco's modified eagle medium (DMEM; catalog number: C0891‐100ml) supplemented with 1% penicillin/streptomycin (catalog number: 15070063) and 10% fetal bovine serum (FBS; catalog number: 26140079) in an incubator at 37°C and 5% CO 2 .

    Techniques: Cell Function Assay, Quantitative RT-PCR, CCK-8 Assay, Migration, Transwell Assay, Flow Cytometry, Concentration Assay, Enzyme-linked Immunosorbent Assay

    miR‐424‐5p reversed the role of SNHG12 in vascular endothelial cell function. (a) miR‐424‐5p levels in HUVECs. (b) Cell viability of HUVECs after mediating SNHG12 and miR‐424‐5p. (c) Cell migration of HUVECs after mediating SNHG12 and miR‐424‐5p. (d) Cell apoptosis of HUVECs after mediating SNHG12 and miR‐424‐5p. (e) Concentration of inflammatory cytokines including TNF‐α, IL‐6, and IL‐1β in the culture supernatant of HUVECs after mediating SNHG12 and miR‐424‐5p. (f) Concentration of adhesion factors, namely SELP, VCAM‐1, and ICAM‐1 in the culture supernatant of HUVECs after mediating SNHG12 and miR‐424‐5p. *** p < 0.001 versus untreated group; ### p < 0.001 versus si‐SNHG12 group.

    Journal: Clinical and Translational Science

    Article Title: Clinical significance and underlying mechanism of long non‐coding RNA SNHG12 in lower extremity deep venous thrombosis

    doi: 10.1111/cts.70023

    Figure Lengend Snippet: miR‐424‐5p reversed the role of SNHG12 in vascular endothelial cell function. (a) miR‐424‐5p levels in HUVECs. (b) Cell viability of HUVECs after mediating SNHG12 and miR‐424‐5p. (c) Cell migration of HUVECs after mediating SNHG12 and miR‐424‐5p. (d) Cell apoptosis of HUVECs after mediating SNHG12 and miR‐424‐5p. (e) Concentration of inflammatory cytokines including TNF‐α, IL‐6, and IL‐1β in the culture supernatant of HUVECs after mediating SNHG12 and miR‐424‐5p. (f) Concentration of adhesion factors, namely SELP, VCAM‐1, and ICAM‐1 in the culture supernatant of HUVECs after mediating SNHG12 and miR‐424‐5p. *** p < 0.001 versus untreated group; ### p < 0.001 versus si‐SNHG12 group.

    Article Snippet: Human vascular endothelial cell (HUVEC; catalog number: PCS‐100‐010) was gained from American Type Culture Collection (ATCC) and maintained in Dulbecco's modified eagle medium (DMEM; catalog number: C0891‐100ml) supplemented with 1% penicillin/streptomycin (catalog number: 15070063) and 10% fetal bovine serum (FBS; catalog number: 26140079) in an incubator at 37°C and 5% CO 2 .

    Techniques: Cell Function Assay, Migration, Concentration Assay