Hamster Proximal Tubular Epithelial Cells

Cat.No.: CSC-C9207J

Species: Hamster

Source: Kidney

Cell Type: Epithelial Cell

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Cat.No.
CSC-C9207J
Description
Hamster Proximal Tubular Epithelial Cells from Creative Bioarray are isolated from proximal tubular tissue of pathogen-free laboratory mice. Hamster Proximal Tubular Epithelial Cells are grown in a T25 tissue culture flask pre-coated with gelatin-based coating solution for 2 min and incubated in Creative Bioarray’s Culture Complete Growth Medium for 3-5 days. Cells are detached from flasks and immediately cryo-preserved in vials. Each vial contains at least 0.5x10^6 cells per ml and is delivered frozen. Cells can be expanded for 3-7 passages at a split ratio of 1:2 under the cell culture conditions specified by Creative Bioarray. Repeated freezing and thawing of cells is not recommended.
Species
Hamster
Source
Kidney
Recommended Medium
Complete Epithelial Cell Medium
Cell Type
Epithelial Cell
Disease
Normal
Storage and Shipping
We ship frozen cells on dry ice. Upon receiving, directly and immediately transfer the cells from dry ice to liquid nitrogen and keep the cells in liquid nitrogen until they are needed for experiments. Never can primary 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.

Hamster proximal tubular epithelial cells (RPTECs) are primary renal epithelial cells isolated from the proximal tubules of the kidney, most often from the Syrian hamster. These cells closely resemble the physiological structure and function of the renal proximal tubule, including active reabsorption, ion transport and metabolic activity. They show characteristic epithelial morphology, form tight junctions and express major transporters, such as Na⁺/K⁺-ATPase, and markers, like megalin and aquaporins.

One of the distinctive features of hamster RPTECs is that they are derived from a hibernating species, which gives them remarkable resistance to hypoxia, oxidative stress and ischemia-reperfusion injury. Compared to rodent or human renal epithelial models, these cells exhibit greater mitochondrial stability, reduced reactive oxygen species (ROS)-induced damage, and a lessened cellular senescence response to stress. Thus, they represent a useful in vitro model to study tolerance to renal injury and adaptive metabolic regulation. Hamster RPTECs are commonly used for acute kidney injury (AKI), oxidative stress mechanisms, nephrotoxicity screening, and renal metabolism. They are also well suited to study protective signaling pathways such as the Nrf2-mediated antioxidant responses and ferroptosis resistance. In summary, these cells offer a unique and physiologically relevant platform to study kidney function and resilience to injury beyond the traditional mammalian models.

Differential Responses of RPTECs to Anoxia-Reoxygenation

Ischemia-reperfusion (I/R) injury is a leading cause of acute kidney injury (AKI), yet effective treatments are lacking. Hibernating mammals, however, show remarkable resistance to I/R-induced cell death. While cellular senescence is a key factor in AKI, its role in this context remains understudied in these species. To explore potential therapeutic insights, Pissas et al. subjected renal proximal tubular epithelial cells (RPTECs) from the hibernating Syrian hamster and the mouse to anoxia-reoxygenation.

Anoxia-reoxygenation significantly increased ROS production in mouse RPTECs (Fig. 1A) and elevated levels of 4-hydroxynonenal (4-HNE)-modified proteins, a marker of lipid peroxidation (Fig. 1B and C). Lactate dehydrogenase (LDH) release confirmed cell death in these cells (Fig. 1D). Similarly, hamster RPTECs exhibited increased ROS (Fig. 1E) and 4-HNE modification (Fig. 1F and G) following anoxia-reoxygenation. In contrast to mice, however, hamster RPTECs showed no significant cell death (Fig. 1H).

Anoxia-reoxygenation increases ROS and lipid peroxidation in both mouse and hamster RPTECs, but hamster cells survive.

Fig. 1. Anoxia-reoxygenation increases ROS and lipid peroxidation in both mouse and hamster RPTECs, but hamster cells survive (Pissas G, Divani M, et al., 2025).

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