Immortalized Human Retinal Microvascular Endothelial Cells-SV40T

Immortalized Human Retinal Microvascular Endothelial Cells-SV40T

Cat.No.: CSC-I2309Z

Species: homo sapiens

Morphology: Polygonal

Culture Properties: Adherent

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Cat.No.
CSC-I2309Z
Description
Immortalized Human Retinal Microvascular Endothelial Cells-SV40T have been obtained immortalizing Human Retinal Microvascular Endothelial Cells with SV40T gene. Immortalized cells were controlled passaging side by side with the primary cells. Primary cells go into senescence after the 4th passage while the SV40 genetranduced cells go beyond 20 passages. This cell line is a great in vitro model system.
Species
homo sapiens
Tissue of Origin
Retina
Recommended Medium
SuperCult® Immortalized Human Retinal Microvascular Endothelial Cell Medium (Cat No.: CM-I2309Z)
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.
Storage
Store in liquid nitrogen
Shipping
Ship in 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
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 retinal microvascular endothelial cells-SV40T (HRMEC/SV40T) are generated by introducing the SV40 large T antigen into primary human retinal microvascular endothelial cells. This confers indefinite proliferative capacity while preserving core endothelial features, including CD31/PECAM-1, VE-cadherin, VEGFR2, and CD34, as well as blood-retinal barrier (BRB)-associated junctional proteins such as claudin-5, occludin, and ZO-1. Functionally, they respond to VEGF and inflammatory stimuli and support proliferation, migration, tube formation, and barrier assays.

Compared with primary HRMECs, HRMEC/SV40T offer a continuous, scalable, and cost-effective source with high batch-to-batch consistency and reduced donor variability. This enables reproducible high-throughput screening, gene perturbation (siRNA/CRISPR), and long-term studies. They are widely used to model retinal angiogenesis and BRB dysfunction in diabetic retinopathy, retinopathy of prematurity, retinal vein occlusion, and macular edema, and to evaluate anti-VEGF agents, corticosteroids, and metabolic or inflammatory modulators.

Limitations: SV40 large T antigen inactivates p53 and Rb and may alter stress/apoptosis responses, barrier tightness, and karyotype. Results should therefore be validated against low-passage primary HRMECs when physiological fidelity is critical. Overall, HRMEC/SV40T provide a practical, human-relevant, and reproducible platform for retinal vascular biology and translational drug discovery.

Involvement of the miR-128-3p in High Glucose-Induced Inflammatory Injury in Retinal Endothelial Cells

This study explores the regulatory mechanism of the miR-128-3p in diabetic retinopathy (DR)-associated inflammatory injury. A cellular model of DR was established by inducing immortalized human retinal endothelial cells (IM-HRECs) with high-glucose (HG). Cell viability was evaluated by CCK-8 assay, and the levels of TNF-α, IL-1β, and IL-10 were measured by ELISA. RT-qPCR was performed to determine miR-128-3p expression, and miR-128-3p mimics were transfected into cells to verify its regulatory role in DR-associated inflammatory injury. The results revealed that HG treatment significantly reduced both IM-HREC viability and IL-10 levels, increased the levels of TNF-α and IL-1β, and downregulated the expression of miR-128-3p. Overexpression of miR-128-3p reduced inflammation in IM-HRECs induced by HG.

Overexpression of miR-128-3p alleviates HG-induced DR inflammatory injury.
Fig. 1. Overexpression of miR-128-3p alleviates HG-induced DR inflammatory injury (Wen, Wei‐Ming, et al., 2026).

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