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human umbilical vein endothelial ea hy926 cell lines  (ATCC)


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    ATCC human umbilical vein endothelial ea hy926 cell lines
    Human Umbilical Vein Endothelial Ea Hy926 Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1833 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/endothelial+cell+line+ea+hy926/EA%2Ehy926/pm42298006-50-26-37
    Average 97 stars, based on 1833 article reviews
    human umbilical vein endothelial ea hy926 cell lines - by Bioz Stars, 2026-10
    97/100 stars

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    Related Articles

    Incubation:

    Article Title: Adipocyte extracellular vesicles (AdEVs) promote a proinflammatory and profibrotic profile in human renal and endothelial cells in vitro.
    Article Snippet: OBJECTIVES: In obesity, white adipose tissue (WAT) undergoes hypertrophic and hyperplastic changes that are driven by phenotypical changes in preadipocytes and adipocytes.. WAT also causes a chronic inflammatory state that modifies gene expression and the secretome, including the shedding of adipose-derived extracellular vesicles (AdEVs) into the circulation, which may influence distant cell types and modulate their phenotypes.. AIM: To evaluate the effects of AdEVs on renal and endothelial cells and determine their impact on gene expression related to inflammation, fibrosis, and endothelial function.

    Western Blot:

    Article Title: Adipocyte extracellular vesicles (AdEVs) promote a proinflammatory and profibrotic profile in human renal and endothelial cells in vitro.
    Article Snippet: OBJECTIVES: In obesity, white adipose tissue (WAT) undergoes hypertrophic and hyperplastic changes that are driven by phenotypical changes in preadipocytes and adipocytes.. WAT also causes a chronic inflammatory state that modifies gene expression and the secretome, including the shedding of adipose-derived extracellular vesicles (AdEVs) into the circulation, which may influence distant cell types and modulate their phenotypes.. AIM: To evaluate the effects of AdEVs on renal and endothelial cells and determine their impact on gene expression related to inflammation, fibrosis, and endothelial function.

    Cell Culture:

    Article Title: Chrysotoxine Attenuates Key Atherogenic Processes via Antioxidant, Anti-Inflammatory, and COX-Dependent Antiplatelet Mechanisms
    Article Snippet: .. The human endothelial cell line EA.hy926 (ATCC ® CRL-2922TM, Manassas, VA, USA) was cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% heat-inactivated fetal bovine serum (FBS) and 1% penicillin–streptomycin. ..

    Article Title: Trimethylamine N-oxide (TMAO) disrupts endothelial junction integrity through VE-cadherin Tyr658 phosphorylation in vitro.
    Article Snippet: Trimethylamine n-oxide (317,594) was purchased from Sigma-Aldrich (St. Louis, MO, USA). .. Endothelial cell culture and treatment conditions An immortalized human endothelial cell line EA.hy926 (ATCC CRL 2922, Manassas, VA, USA) was cultured in DMEM supplemented with 10% fetal bovine serum (FBS) and 10 mg/mL of penicillin/streptomycin and maintained at 37 °C in a humidified atmosphere containing 5% CO2. ..

    Article Title: Chrysotoxine Attenuates Key Atherogenic Processes via Antioxidant, Anti-Inflammatory, and COX-Dependent Antiplatelet Mechanisms
    Article Snippet: .. The human endothelial cell line EA.hy926 (ATCC® CRL-2922TM, Manassas, VA, USA) was cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% heat-inactivated fetal bovine serum (FBS) and 1% penicillin–streptomycin. ..

    Modification:

    Article Title: Chrysotoxine Attenuates Key Atherogenic Processes via Antioxidant, Anti-Inflammatory, and COX-Dependent Antiplatelet Mechanisms
    Article Snippet: .. The human endothelial cell line EA.hy926 (ATCC ® CRL-2922TM, Manassas, VA, USA) was cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% heat-inactivated fetal bovine serum (FBS) and 1% penicillin–streptomycin. ..

    Article Title: Chrysotoxine Attenuates Key Atherogenic Processes via Antioxidant, Anti-Inflammatory, and COX-Dependent Antiplatelet Mechanisms
    Article Snippet: .. The human endothelial cell line EA.hy926 (ATCC® CRL-2922TM, Manassas, VA, USA) was cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% heat-inactivated fetal bovine serum (FBS) and 1% penicillin–streptomycin. ..



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    Arg169 symmetric dimethylation is required for SHBs–driven angiogenesis and tumor growth. (A) WB analysis of SHBs and BIP expression in stably transduced Huh7 and HepG2 cells (Vector, SHBs, and SHBs/R169K). (B) ELISA measurement of VEGFA levels in the supernatants of Huh7/HepG2–Vector, Huh7/HepG2–SHBs, or Huh7/HepG2–SHBs/R169K cells. (C) Endothelial tube formation <t>assay.</t> <t>EA.hy926</t> cells were cultured with conditioned media (CM) from Huh7 or HepG2 stable lines (Vector, SHBs, SHBs/R169K). Representative images and quantification of mesh numbers are shown. (D) Transwell migration assay. EA.hy926 cells were assessed for migration in response to CM from the indicated stable lines. Representative images and quantification of migrated cell numbers per field are shown. (E) Representative images of excised subcutaneous xenograft tumors derived from Huh7–Vector, Huh7–SHBs, or Huh7–SHBs/R169K cells. (F) Tumor growth curves (tumor volume over time) for the indicated xenograft groups. (G) Tumor weights at endpoint. (H) Representative immunohistochemical staining of xenograft tumors for CD31 and SHBs, with quantification of microvessel density (MVD) based on CD31 staining. Data are presented as mean ± SD; ∗ P < 0.05 as indicated.
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    Arg169 symmetric dimethylation is required for SHBs–driven angiogenesis and tumor growth. (A) WB analysis of SHBs and BIP expression in stably transduced Huh7 and HepG2 cells (Vector, SHBs, and SHBs/R169K). (B) ELISA measurement of VEGFA levels in the supernatants of Huh7/HepG2–Vector, Huh7/HepG2–SHBs, or Huh7/HepG2–SHBs/R169K cells. (C) Endothelial tube formation <t>assay.</t> <t>EA.hy926</t> cells were cultured with conditioned media (CM) from Huh7 or HepG2 stable lines (Vector, SHBs, SHBs/R169K). Representative images and quantification of mesh numbers are shown. (D) Transwell migration assay. EA.hy926 cells were assessed for migration in response to CM from the indicated stable lines. Representative images and quantification of migrated cell numbers per field are shown. (E) Representative images of excised subcutaneous xenograft tumors derived from Huh7–Vector, Huh7–SHBs, or Huh7–SHBs/R169K cells. (F) Tumor growth curves (tumor volume over time) for the indicated xenograft groups. (G) Tumor weights at endpoint. (H) Representative immunohistochemical staining of xenograft tumors for CD31 and SHBs, with quantification of microvessel density (MVD) based on CD31 staining. Data are presented as mean ± SD; ∗ P < 0.05 as indicated.
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    Image Search Results


    Arg169 symmetric dimethylation is required for SHBs–driven angiogenesis and tumor growth. (A) WB analysis of SHBs and BIP expression in stably transduced Huh7 and HepG2 cells (Vector, SHBs, and SHBs/R169K). (B) ELISA measurement of VEGFA levels in the supernatants of Huh7/HepG2–Vector, Huh7/HepG2–SHBs, or Huh7/HepG2–SHBs/R169K cells. (C) Endothelial tube formation assay. EA.hy926 cells were cultured with conditioned media (CM) from Huh7 or HepG2 stable lines (Vector, SHBs, SHBs/R169K). Representative images and quantification of mesh numbers are shown. (D) Transwell migration assay. EA.hy926 cells were assessed for migration in response to CM from the indicated stable lines. Representative images and quantification of migrated cell numbers per field are shown. (E) Representative images of excised subcutaneous xenograft tumors derived from Huh7–Vector, Huh7–SHBs, or Huh7–SHBs/R169K cells. (F) Tumor growth curves (tumor volume over time) for the indicated xenograft groups. (G) Tumor weights at endpoint. (H) Representative immunohistochemical staining of xenograft tumors for CD31 and SHBs, with quantification of microvessel density (MVD) based on CD31 staining. Data are presented as mean ± SD; ∗ P < 0.05 as indicated.

    Journal: Tumour Virus Research

    Article Title: PRMT5–mediated symmetric dimethylation of SHBs at Arg169 stabilizes SHBs and promotes angiogenesis and tumor growth

    doi: 10.1016/j.tvr.2026.200340

    Figure Lengend Snippet: Arg169 symmetric dimethylation is required for SHBs–driven angiogenesis and tumor growth. (A) WB analysis of SHBs and BIP expression in stably transduced Huh7 and HepG2 cells (Vector, SHBs, and SHBs/R169K). (B) ELISA measurement of VEGFA levels in the supernatants of Huh7/HepG2–Vector, Huh7/HepG2–SHBs, or Huh7/HepG2–SHBs/R169K cells. (C) Endothelial tube formation assay. EA.hy926 cells were cultured with conditioned media (CM) from Huh7 or HepG2 stable lines (Vector, SHBs, SHBs/R169K). Representative images and quantification of mesh numbers are shown. (D) Transwell migration assay. EA.hy926 cells were assessed for migration in response to CM from the indicated stable lines. Representative images and quantification of migrated cell numbers per field are shown. (E) Representative images of excised subcutaneous xenograft tumors derived from Huh7–Vector, Huh7–SHBs, or Huh7–SHBs/R169K cells. (F) Tumor growth curves (tumor volume over time) for the indicated xenograft groups. (G) Tumor weights at endpoint. (H) Representative immunohistochemical staining of xenograft tumors for CD31 and SHBs, with quantification of microvessel density (MVD) based on CD31 staining. Data are presented as mean ± SD; ∗ P < 0.05 as indicated.

    Article Snippet: Human hepatoma cell lines HepG2 (ATCC, HB–8065) and Huh7 (JCRB, JCRB0403), endothelial cell line EA.hy926 (ATCC, CRL–2922TM), and HEK293T cells (ATCC, CRL–3216) were obtained from the American Type Culture Collection (ATCC) and the Japanese Collection of Research Bioresources Cell Bank (JCRB, Japan).

    Techniques: Expressing, Stable Transfection, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Endothelial Tube Formation Assay, Cell Culture, Transwell Migration Assay, Migration, Derivative Assay, Immunohistochemical staining, Staining