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primary umbilical vein endothelial cells; normal, human, pooled  (ATCC)


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    ATCC primary umbilical vein endothelial cells; normal, human, pooled
    Primary Umbilical Vein Endothelial Cells; Normal, Human, Pooled, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1307 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary umbilical vein endothelial cells; normal, human, pooled/product/ATCC
    Average 99 stars, based on 1307 article reviews
    primary umbilical vein endothelial cells; normal, human, pooled - by Bioz Stars, 2026-05
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    ATCC human umbilical vein endothelial cells
    Effects of Na/K conditions and antihypertensive treatments on <t>endothelial</t> injury in HUVECs. (A) Cell viability assessed by CCK-8. (B) Intracellular ROS detected by DCFH-DA fluorescence. (C) NO levels determined by Griess assay. (D) ET-1 levels determined by ELISA. (E) Western blot analysis of eNOS and ICAM-1 expression; β-actin served as loading control. *** P < 0.001 vs. Control group. ### P < 0.001 vs. Ang II group.
    Human Umbilical Vein Endothelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human umbilical vein endothelial cells/product/ATCC
    Average 99 stars, based on 1 article reviews
    human umbilical vein endothelial cells - by Bioz Stars, 2026-05
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    ATCC human umbilical vein endothelial cells huvecs
    Regulatory role of HSPB1 in <t>endothelial</t> cell EndoMT (A) Western blot shows HSPB1 expression in <t>HUVECs</t> following lentiviral-mediated overexpression (LV-HSPB1) or knockdown (LV-HSPB1-RNAi); β-actin served as a loading control. (B) Quantification of HSPB1/β-actin ratio shows significant differences between groups. (C) Representative images of Transwell migration assays evaluating the effect of HSPB1 on TGF-β1–induced endothelial migration (scale bars, 100 μm). (D) Quantification of migrated cells per field. (E) Representative tube formation images showing the effect of HSPB1 modulation on TGF-β1–induced angiogenic activity (scale bars, 200 μm). (F–H) Quantitative analysis of tube formation parameters, including the number of branches (F), loops (G), and total tube length (H), measured using ImageJ software. Data are presented as mean ± SD ( n ≥ 6). Exact p values are indicated in the graphs. Statistical analyses were performed using one-way ANOVA followed by a Bonferroni post hoc test.
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    huvec  (ATCC)
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    ATCC huvec
    Regulatory role of HSPB1 in <t>endothelial</t> cell EndoMT (A) Western blot shows HSPB1 expression in <t>HUVECs</t> following lentiviral-mediated overexpression (LV-HSPB1) or knockdown (LV-HSPB1-RNAi); β-actin served as a loading control. (B) Quantification of HSPB1/β-actin ratio shows significant differences between groups. (C) Representative images of Transwell migration assays evaluating the effect of HSPB1 on TGF-β1–induced endothelial migration (scale bars, 100 μm). (D) Quantification of migrated cells per field. (E) Representative tube formation images showing the effect of HSPB1 modulation on TGF-β1–induced angiogenic activity (scale bars, 200 μm). (F–H) Quantitative analysis of tube formation parameters, including the number of branches (F), loops (G), and total tube length (H), measured using ImageJ software. Data are presented as mean ± SD ( n ≥ 6). Exact p values are indicated in the graphs. Statistical analyses were performed using one-way ANOVA followed by a Bonferroni post hoc test.
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    ATCC dmem medium
    Regulatory role of HSPB1 in <t>endothelial</t> cell EndoMT (A) Western blot shows HSPB1 expression in <t>HUVECs</t> following lentiviral-mediated overexpression (LV-HSPB1) or knockdown (LV-HSPB1-RNAi); β-actin served as a loading control. (B) Quantification of HSPB1/β-actin ratio shows significant differences between groups. (C) Representative images of Transwell migration assays evaluating the effect of HSPB1 on TGF-β1–induced endothelial migration (scale bars, 100 μm). (D) Quantification of migrated cells per field. (E) Representative tube formation images showing the effect of HSPB1 modulation on TGF-β1–induced angiogenic activity (scale bars, 200 μm). (F–H) Quantitative analysis of tube formation parameters, including the number of branches (F), loops (G), and total tube length (H), measured using ImageJ software. Data are presented as mean ± SD ( n ≥ 6). Exact p values are indicated in the graphs. Statistical analyses were performed using one-way ANOVA followed by a Bonferroni post hoc test.
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    Image Search Results


    Effects of Na/K conditions and antihypertensive treatments on endothelial injury in HUVECs. (A) Cell viability assessed by CCK-8. (B) Intracellular ROS detected by DCFH-DA fluorescence. (C) NO levels determined by Griess assay. (D) ET-1 levels determined by ELISA. (E) Western blot analysis of eNOS and ICAM-1 expression; β-actin served as loading control. *** P < 0.001 vs. Control group. ### P < 0.001 vs. Ang II group.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Is the effect of antihypertensive drug therapy on blood pressure control and prevalent cardiovascular disease associated with dietary sodium-potassium ratio? A cross-sectional study based on NHANES

    doi: 10.3389/fcvm.2026.1763612

    Figure Lengend Snippet: Effects of Na/K conditions and antihypertensive treatments on endothelial injury in HUVECs. (A) Cell viability assessed by CCK-8. (B) Intracellular ROS detected by DCFH-DA fluorescence. (C) NO levels determined by Griess assay. (D) ET-1 levels determined by ELISA. (E) Western blot analysis of eNOS and ICAM-1 expression; β-actin served as loading control. *** P < 0.001 vs. Control group. ### P < 0.001 vs. Ang II group.

    Article Snippet: To complement the population-level findings and explore potential mechanisms underlying the associations observed in the NHANES analysis, we established an in vitro endothelial injury model using human umbilical vein endothelial cells (HUVECs, ATCC, PCS-100-013).

    Techniques: CCK-8 Assay, Fluorescence, Griess Assay, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Control

    Regulatory role of HSPB1 in endothelial cell EndoMT (A) Western blot shows HSPB1 expression in HUVECs following lentiviral-mediated overexpression (LV-HSPB1) or knockdown (LV-HSPB1-RNAi); β-actin served as a loading control. (B) Quantification of HSPB1/β-actin ratio shows significant differences between groups. (C) Representative images of Transwell migration assays evaluating the effect of HSPB1 on TGF-β1–induced endothelial migration (scale bars, 100 μm). (D) Quantification of migrated cells per field. (E) Representative tube formation images showing the effect of HSPB1 modulation on TGF-β1–induced angiogenic activity (scale bars, 200 μm). (F–H) Quantitative analysis of tube formation parameters, including the number of branches (F), loops (G), and total tube length (H), measured using ImageJ software. Data are presented as mean ± SD ( n ≥ 6). Exact p values are indicated in the graphs. Statistical analyses were performed using one-way ANOVA followed by a Bonferroni post hoc test.

    Journal: iScience

    Article Title: Cardiomyocyte-derived HSPB1 regulates TGF-β1 maturation and inhibits endothelial-to-mesenchymal transition in myocardial fibrosis

    doi: 10.1016/j.isci.2026.115028

    Figure Lengend Snippet: Regulatory role of HSPB1 in endothelial cell EndoMT (A) Western blot shows HSPB1 expression in HUVECs following lentiviral-mediated overexpression (LV-HSPB1) or knockdown (LV-HSPB1-RNAi); β-actin served as a loading control. (B) Quantification of HSPB1/β-actin ratio shows significant differences between groups. (C) Representative images of Transwell migration assays evaluating the effect of HSPB1 on TGF-β1–induced endothelial migration (scale bars, 100 μm). (D) Quantification of migrated cells per field. (E) Representative tube formation images showing the effect of HSPB1 modulation on TGF-β1–induced angiogenic activity (scale bars, 200 μm). (F–H) Quantitative analysis of tube formation parameters, including the number of branches (F), loops (G), and total tube length (H), measured using ImageJ software. Data are presented as mean ± SD ( n ≥ 6). Exact p values are indicated in the graphs. Statistical analyses were performed using one-way ANOVA followed by a Bonferroni post hoc test.

    Article Snippet: Human umbilical vein endothelial cells (HUVECs) , ATCC , Primary cells, pooled donors.

    Techniques: Western Blot, Expressing, Over Expression, Knockdown, Control, Migration, Activity Assay, Software

    Effects of HSPB1 on signaling pathways and TGF-β secretion in HUVECs under hypoxic conditions (A and B) HUVECs were transfected with adenoviral vectors for HSPB1 overexpression (OE) or knockdown (KD) and cultured for 48 h before RNA extraction. Gene expression analysis was performed using RNA sequencing. Gene set enrichment analysis (GSEA) assessed the regulatory roles of HSPB1 in processes such as heart development, angiogenesis, and cell proliferation (A). Further analysis using Hallmark gene sets explored HSPB1 signaling pathway activation (B). (C–G) Following transfection, HUVECs were cultured for 24 h and subjected to hypoxic conditions (3% O 2 ) for 48 h. Western blot analysis of the indicated proteins was performed. (D) pSmad2/3/Smad2/3 ratio, (E) quantification of CD31 protein expression, (F) quantification of E-cadherin expression, (G) quantification of α-SMA expression, and (H) quantification of N-cadherin expression were measured relative to β-actin. (I) TGF-β levels were measured by ELISA in cell supernatants. Data are presented as mean ± SD ( n ≥ 6). Exact p values are indicated in the graphs. Statistical analyses were performed using one-way ANOVA followed by a Bonferroni post hoc test.

    Journal: iScience

    Article Title: Cardiomyocyte-derived HSPB1 regulates TGF-β1 maturation and inhibits endothelial-to-mesenchymal transition in myocardial fibrosis

    doi: 10.1016/j.isci.2026.115028

    Figure Lengend Snippet: Effects of HSPB1 on signaling pathways and TGF-β secretion in HUVECs under hypoxic conditions (A and B) HUVECs were transfected with adenoviral vectors for HSPB1 overexpression (OE) or knockdown (KD) and cultured for 48 h before RNA extraction. Gene expression analysis was performed using RNA sequencing. Gene set enrichment analysis (GSEA) assessed the regulatory roles of HSPB1 in processes such as heart development, angiogenesis, and cell proliferation (A). Further analysis using Hallmark gene sets explored HSPB1 signaling pathway activation (B). (C–G) Following transfection, HUVECs were cultured for 24 h and subjected to hypoxic conditions (3% O 2 ) for 48 h. Western blot analysis of the indicated proteins was performed. (D) pSmad2/3/Smad2/3 ratio, (E) quantification of CD31 protein expression, (F) quantification of E-cadherin expression, (G) quantification of α-SMA expression, and (H) quantification of N-cadherin expression were measured relative to β-actin. (I) TGF-β levels were measured by ELISA in cell supernatants. Data are presented as mean ± SD ( n ≥ 6). Exact p values are indicated in the graphs. Statistical analyses were performed using one-way ANOVA followed by a Bonferroni post hoc test.

    Article Snippet: Human umbilical vein endothelial cells (HUVECs) , ATCC , Primary cells, pooled donors.

    Techniques: Protein-Protein interactions, Transfection, Over Expression, Knockdown, Cell Culture, RNA Extraction, Gene Expression, RNA Sequencing, Activation Assay, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay