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Immortalized Human Urothelial Cells

Cat.No.: CSC-I9089L

Species: Homo sapiens

Source: Urinary Bladder

Morphology: Epithelial-like

Culture Properties: Adherent

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Cat.No.
CSC-I9089L
Species
Homo sapiens
Source
Urinary Bladder
Culture Properties
Adherent
Morphology
Epithelial-like
Markers
Cytokeratin-18, cytokeratin-19, vimentin
Applications
For Research Use Only
Storage
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.
Shipping
Dry Ice.
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BioSafety Level
II
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.

Researchers developed SV40-Immortalized Human Urothelial Cells (SV-HUC) by introducing the SV40 large T-antigen gene from Simian Virus 40 into human urothelial cells. Human urothelial cells form an epithelial layer that lines the bladder and other urinary organs like ureters and renal pelvis. The urothelial cells function as a protective barrier against external pathogens in the urinary system while also participating in urine formation and excretion processes.

SV-HUC enable researchers to study urinary system diseases and develop drugs while also analyzing gene functions. For instance, gene editing technologies utilize these cells to analyze the effects of oncogenic mutations on cellular behavior. Researchers conduct carcinogenicity and toxicity assessments of various compounds by exposing these cells to substances like p-phenylenediamine. Additionally, researchers use these cells to study how low-dose radiation affects human cells particularly concerning the development of bladder cancer.

Electron microscopy images of SV-40 immortalized human urothelial cells.Fig. 1. Electron microscopy images of SV-40 immortalized human urothelial cells (SV-HUC-1 cells) (Luo HJ, Zhou H, et al., 2024).

PPD Induced EMT in SV-HUC-1 Cells

Bladder cancer rates are increasing with PPD being a suspect carcinogen due to its presence in various consumer and industrial products. Epidemiological evidence links PPD exposure to multiple cancers. Liu's team studied PPD's potential in inducing EMT in SV-40 immortalized human urothelial cells through the ERK5/AP-1 pathway.

PPD was used on immortalized human urothelial cell line SV-40 (SV-HUC-1) to explore its relationship with bladder cancer. At concentrations between 0 and 5 µM, PPD showed no toxicity to cell viability (Fig. 1A). For further experiments, concentrations of 0.002, 0.01, and 0.05 µM were selected. EMT is marked by changes in cell shape, invasion, and migration. After PPD treatment, cells showed morphological changes, stretching into a spindle shape with pseudopodium formation (Fig. 1B). The wound healing and transwell assays demonstrated that the cells' migration and invasion abilities improved (Fig. 1C and D). Dose-dependent decreases in epithelial markers E-cadherin and ZO-1 were observed alongside increases in mesenchymal markers N-cadherin and vimentin through Western blotting results (Fig. 1E). qRT-PCR confirmed these mRNA expression changes (Fig. 1F). Immunofluorescence staining displayed cellular alterations caused by PPD treatment (Fig. 1G). The results demonstrate that PPD triggers EMT in SV-HUC-1 cells.

PPD induces EMT in SV-40 immortalized human urothelial cells.Fig. 1. PPD induces EMT in SV-HUC-1 cells (Liu ZQ, Zhao L, et al., 2022).

Hypoxia Down-Regulated the mRNA Expression of TJ- Proteins and Damaged TJ Structure in SV-HUC-1 Cells

Hypoxia plays an important role in the pathological process of bladder outlet obstruction. Previous research has mostly focused on the dysfunction of bladder smooth muscle cells, which are directly related to bladder contraction. Liu's team delved into the barrier function changes of the urothelial cells under exposure to hypoxia.

To assess hypoxia's impact on barrier-forming proteins, qPCR measured mRNA levels of AUM (UPIa, UPIb, UPII, UPIIIa) and TJ proteins (ZO-1, claudin1, occludin) in SV-40 immortalized human urothelial cells (SV-HUC-1). Short 2-hour oxygen deprivation didn't affect TJ protein expression, but 24-hour hypoxia significantly reduced ZO-1, claudin, and occludin mRNA (Fig. 2A-C). AUM protein levels remained unchanged (Fig. 2D-G). WB assay further detected the protein level of AUM proteins and TJ-associated proteins. Results revealed that 24-hour hypoxia and beyond substantially decreased TJ protein levels, with occludin showing the greatest reduction. AUM protein expression, including UPIa, UPIb, UPII, and UPIIIa, was largely stable. Immunofluorescence showed increased expression of TJ proteins. However, hypoxia reduced ZO-1, claudin-1, and occludin expression at cell junctions (Fig. 3).

Impact of hypoxia on expression of genes related to urothelial barrier.Fig. 2. Effect of hypoxia on the urothelial barrier-related gene expression (Liu HJ, Zhou H, et al., 2024).

Immunofluorescent staining of ZO-1, claudin-1 and occludin proteins under hypoxia exposure.Fig. 3. Immunofluorescent staining of ZO-1, claudin-1 and occludin proteins under exposure to hypoxia (Liu HJ, Zhou H, et al., 2024).

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