Immortalized Human Umbilical Vein Endothelial Cells (SV40)-GFP

Immortalized Human Umbilical Vein Endothelial Cells (SV40)-GFP

Cat.No.: CSC-I2045Z

Species: homo sapiens

Morphology: Polygonal

Culture Properties: Adherent

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Cat.No.
CSC-I2045Z
Description
Primary human umbilical vein endothelial cells were isolated and transfected with SV40LT and GFP expressing lentiviral particles. Immortalized Human Umbilical Vein Endothelial Cells (SV40)-GFP from Creative Bioarray go beyond 30 passages.
Species
homo sapiens
Recommended Medium
SuperCult® Immortalized Human Umbilical Vein Endothelial Cell Medium (Cat No.: CM-I2045Z)
Freezing Medium
Complete medium supplemented with 10% (v/v) DMSO
Culture Properties
Adherent
Morphology
Polygonal
Immortalization Method
SV40 large T antigen
Application
For Research Use Only
Growth Properties
Cells are cultured as a monolayer at 37°C in a humidified atmosphere with 5% CO2.
Shipping
Dry Ice.
Quality Control
Real Time PCR was used to quantify SV40T gene expression in immortalized cell line.
free from contaminations (bacteria incl. mycoplasma, fungi, HIV, HAV, HBV, HCV, Parvo-B19) and cross-contaminations
Storage and Shipping
Directly and immediately transfer cells from dry ice to liquid nitrogen upon receiving and keep the cells in liquid nitrogen until cell culture needed for experiments.

Note: Never can cells be kept at -20°C.
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

Immortalized human umbilical vein endothelial cells (SV40)-GFP (HUVEC/SV40-GFP) are generated by introducing the SV40 large T antigen into primary HUVECs, followed by stable expression of green fluorescent protein (GFP). The SV40 T antigen confers indefinite proliferative capacity, while GFP provides a constitutive, non-invasive fluorescent label. Together, these features yield a scalable, trackable, and reproducible endothelial model.

The cells typically retain core endothelial markers, including CD31/PECAM-1, VE-cadherin, VEGFR2, CD34, von Willebrand factor, and eNOS. Functionally, they respond to VEGF and inflammatory cytokines and support proliferation, migration, tube formation, acetylated LDL uptake, barrier assays, leukocyte adhesion, and nitric oxide signaling. GFP expression enables real-time visualization, fluorescence-activated cell sorting, accurate quantification, and live-cell tracking in co-culture and 3D systems.

Compared with primary HUVECs, HUVEC/SV40-GFP overcome limited lifespan and donor variability, providing continuous supply, high batch consistency, and cost-effective expansion for high-throughput screening, siRNA/CRISPR perturbation, and long-term studies. They are widely used in angiogenesis, vascular permeability, inflammation, atherosclerosis, thrombosis, and endothelial dysfunction research, as well as drug discovery, target validation, toxicity testing, and host–pathogen studies. GFP labeling further facilitates co-culture with tumor cells, immune cells, or fibroblasts and supports imaging-based assays.

Uratylated Albumin Activates Endothelial Cells to Induce Monocyte Adhesion and The Release of Pro-Inflammatory Cytokines

Previous studies have demonstrated a link between uric acid (UA) oxidation products, particularly urate hydroperoxide (HOOU), and albumin modifications through a process termed uratylation. Therefore, the aim of this study was to investigate the structural and functional consequences of uratylation on albumin and its effects on endothelial cells. Uratylation promotes a decrease in enthalpy change of denaturation of albumin and binding of Anilino-Naphthalene-Sulfonic acid (ANS), suggesting slight changes in protein structure. Uratylated albumin reduced human umbilical vein endothelial cell (HUVEC) migration, increased intercellular adhesion molecule-1 (ICAM-1) expression and, consequently, monocyte adhesion (THP-1), indicating endothelial activation. Furthermore, the presence of uratylated albumin stimulated the release of tumor necrosis factor-α (TNF-α). These findings provide novel insights into the mechanistic pathways connecting uric acid oxidation, post-translational modification on albumin and inflammation, highlighting the potential role of uratylated albumin in endothelial dysfunction and atherogenesis.

Uratylated albumin activate HUVECs and stimulate monocytes adhesion to them.
Fig. 1. Uratylated albumin increases monocyte adhesion to endothelial cells (da Silva, Railmara P., et al., 2026).
Uratylated albumin induces the release of TNF-α.
Fig. 2. Uratylated albumin induced TNF-α (da Silva, Railmara P., et al., 2026).

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