Immortalized Mouse Hepatocytes-SV40
Cat.No.: CSC-I2205Z
Species: mouse
Morphology: Polygonal
Culture Properties: Adherent
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free from contaminations (bacteria incl. mycoplasma, fungi, HIV, HAV, HBV, HCV, Parvo-B19) and cross-contaminations
Note: Never can cells be kept at -20°C.
Immortalized Mouse Hepatocytes-SV40 are derived from C57BL/6 mouse liver and engineered for continuous proliferation via lentiviral transduction of SV40 large T antigen, with transgene expression validated by real-time PCR. These adherent, polygonal cells overcome the fundamental limitation of primary hepatocytes—rapid onset of replicative senescence after the first passage—by maintaining robust growth beyond 20 passages without loss of viability or phenotypic integrity.
Compared to conventional hepatoma lines, this immortalized model retains closer fidelity to native hepatic biology while offering unlimited experimental scalability. The cells provide a renewable, genetically stable platform for investigating hepatocyte biology, hepatic metabolism, stress responses, and disease-associated signaling pathways. Their well-defined C57BL/6 background ensures reproducibility across genetic, transcriptomic, and compound-response studies.
With demonstrated utility in gene expression analysis, drug metabolism, and toxicity screening, Immortalized Mouse Hepatocytes-SV40 bridge the gap between short-lived primary cultures and fully transformed cell lines. They deliver the physiological relevance of hepatocyte-derived models together with the experimental consistency and throughput essential for mechanistic research and preclinical evaluation.
BMP6 Participates in the Molecular Mechanisms Involved in APAP Hepatotoxicity
Given the lack of accurate diagnostic methods of acetaminophen (APAP)-induced acute liver failure (ALF), the search for new biomarkers for its diagnosis is an urgent need. The aim of this study was to evaluate the role of bone morphogenetic protein 6 (BMP6) in APAP-induced ALF progression and its potential value as a biomarker of ALF.
Immortalized neonatal mouse hepatocytes were exposed to APAP (1 mM and 5 mM) for 16 h to assess APAP-induced cell death. As shown in Fig. 1A, we observed a decrease in cell viability in a concentration-dependent manner. Moreover, both APAP concentrations had cytotoxic effects reflected by the release of LDH (Fig. 1B) and presence of apoptotic nuclei (Fig. 1C). Furthermore, we used DHE probe to measure reactive oxygen species (ROS) production in these cells during 2 h after APAP stimulation and we found that APAP-induced ROS (Fig. 1D) and, thus, ROS-mediated JNK and P38 MAPK phosphorylation was also observed (Fig. 1E). Next, we measured Bmp6 mRNA levels and found a significant increase in hepatocytes treated with APAP compared to the controls (Fig. 1F). In addition, BMP6 was detected in the culture media (CM) from cells exposed to APAP (Fig. 1G).

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