Immortalized Mouse Intestinal Epithelial Cells-SV40T
Cat.No.: CSC-I2100Z
Morphology: Polygonal
Culture Properties: Adherent
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Note: Never can cells be kept at -20°C.
Derived from primary mouse intestinal epithelial cells, Immortalized Mouse Intestinal Epithelial Cells-SV40T are murine cell lines modified genetically with the SV40 large T antigen (SV40T) to enhance their proliferative capacity. Immortalization is achieved through the SV40T protein, which inactivates the key tumor suppressors p53 and retinoblastoma (Rb) proteins. When cultured in the laboratory, these cells exhibit adherent growth and a classic cobblestone shape. They form confluent monolayers with tight cell-to-cell connections, a key characteristic of epithelial cells. These cells also express major intestinal epithelial markers, such as E-cadherin, zonula occludens-1 (ZO-1), villin, and cytokeratins-expressions that verify their epithelial origin and functional barrier abilities. With appropriate culture conditions, the cells can further develop polarized epithelial characteristics and sustain functions associated with intestinal absorption and secretion.
These cells are extensively used in functional research, including investigations into intestinal development, the integrity of the epithelial barrier, immune signaling mechanisms, and cellular reactions to microbial pathogens or inflammatory stimuli. They also play an important role in studies related to drug transport, toxicology, and the modeling of intestinal diseases like inflammatory bowel disease and infection biology. Thanks to their stability, reproducibility, and preserved epithelial phenotype, these cells have become a robust platform for basic gastrointestinal research, translational studies, and preclinical applications.
Calycosin Inhibits NLRP3-Induced Inflammation in IBD
Intestinal interstitial fibrosis is a core event in inflammatory bowel disease (IBD) development. Calycosin possesses various therapeutic bioactivities, but its role in intestinal fibrosis remains unclear. Liao et al. explored calycosin's effects on intestinal interstitial fibrosis and underlying mechanisms using TNBS-induced mouse IBD models, co-culture systems of intestinal epithelial and interstitial cells, and lentivirus-mediated NLRP3 knockdown.
Given that inflammation drives intestinal fibrosis in IBD, they first evaluated NLRP3 expression across control, IBD model, and calycosin-treated (CA) groups. NLRP3 mRNA and its downstream targets caspase-1 and IL-1β were significantly elevated in IBD mice compared to controls, but markedly downregulated by calycosin treatment (Fig. 1A). Similarly, fibrosis markers Collagen-1, TIMP-1, and α-SMA were increased in intestinal epithelial cells from IBD animals and reduced by calycosin (Fig. 1B-C). NLRP3 inflammasome components (NLRP3, caspase-1, ASC) showed comparable patterns (Fig. 1D-E). To elucidate NLRP3's role in calycosin's anti-fibrotic effects, NLRP3 was knocked down in MODE-K intestinal epithelial cells. Calycosin upregulated fibrogenic factors (Kgf, Ctg, Fgf2, Tgf-β, Igf-1, Pdgf-b), but this effect was abolished upon NLRP3 knockdown (Fig. 1F). These results indicate that calycosin modulates fibrogenic factor expression in an NLRP3-dependent manner.
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