Immortalized Mouse Hepatocytes-SV40T

Cat.No.: CSC-I2101Z

Morphology: Polygonal

Culture Properties: Adherent

  • Specification
  • Background
  • Scientific Data
  • Q & A
  • Customer Review
Cat.No.
CSC-I2101Z
Description
Immortalized Mouse Hepatocytes-SV40T were developed from mouse tissues transduced with a lentiviral expression vector containing the SV40T gene. The cell line was continuously cultured for more than 30 passages without showing signs of growth retardation or replicative senescence.
Culture Properties
Adherent
Morphology
Polygonal
Shipping
Dry Ice.
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 Mouse Hepatocytes-SV40T, derived from mice, are hepatocytes that have been genetically modified to constitutively express the SV40 large T antigen. The expression of SV40T allows them to circumvent replicative senescence and proliferate indefinitely in vitro.

Immortalized Mouse Hepatocytes-SV40T are polygonal epithelial cells that can be cultured as monolayer adherent cells. They express albumin (Alb), AFP, CK18, HNF-1α, HNF-4α, and sometimes will express functional phase I (CYP450 family members) and phase II (UGTs, GSTs) metabolism enzymes if maintained appropriately. They may also store glycogen, produce urea and respond to certain hormones such as insulin or glucagon. They are commonly utilized for investigations into liver metabolism, metabolism of xenobiotics, hepatitis virus infection, lipid metabolism, liver regeneration, transformation and cytotoxicity studies. They are also utilized for transfection experiments and CRISPR knockout studies.

ER Stress Upregulates S100A11 in Steatohepatitis Models Via Epigenetic Modifications Within the Lipotoxicity-Influenced Enhancer

The pathogenesis of metabolic dysfunction-associated steatohepatitis (MASH) involves lipotoxicity, endoplasmic reticulum (ER) stress, and inflammation. Daniel et al. show that lipotoxicity-induced ER stress epigenetically upregulates the proinflammatory alarmin S100A11 and illuminates how to therapeutically target S100A11.

To determine which DAMPs are enriched in EVs shed by lipotoxic hepatocytes, the authors performed proteomics on EVs secreted by palmitate-treated immortalized mouse hepatocytes (WT-IMH). Bioinformatic processing identified 1660 proteins with altered expression, including 44 DAMPs (Fig. 1A). Of these, S100A11 was the most significantly upregulated protein in palmitate-treated WT-IMH EVs (Fig. 1B). Validation of S100A11 enrichment in EVs was performed using multiple methods. Immunogold EM demonstrated increased cell surface expression of S100A11 on EVs derived from palmitate-treated primary mouse hepatocytes (Fig. 1C). SPR quantification using anti-ASGR1 antibody-captured EVs confirmed S100A11 enrichment on palmitate-stimulated EVs (Fig. 1D). In human Huh7 cells, Western blotting showed increased S100A11 in EV lysates from palmitate-treated cells. ELISA of conditioned supernatants revealed higher S100A11 with palmitate treatment, which disappeared upon EV depletion; isolated EVs confirmed S100A11 enrichment (Fig. 1E). Thus, palmitate-induced lipotoxicity drives release of S100A11-enriched EVs.

S100A11 is enriched in hepatic EVs

Fig. 1. S100A11 is enriched in hepatic EVs (Daniel P V, Erickson H L, et al., 2025).

Ask a Question

Write your own review

For research use only. Not for any other purpose.

Hot Products