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• W2186803608 endingPage "4791" @default.
• W2186803608 startingPage "4785" @default.
• W2186803608 abstract "ABSTRACT Peroxisome proliferators (PPs) cause hepatocyte proliferation and tumorigenesis in rodent liver. PPs induce hepatocyte DNA synthesis although the mechanism is unclear. Tumour necrosis factor α (TNFα) and epidermal growth factor (EGF) have been implicated in mediating this growth response since these factors induce a threefold and 17.2-fold increase, respectively, in DNA synthesis in rat primary hepatocyte cultures. Previously, others have suggested that TNFα acts as a primer to sensitise hepatocytes to the proliferative effects of growth factors. Indeed, here we show that costimulation with TNFα and a suboptimal (4-20% of optimal) concentration of EGF permits an 11.7-fold increase in DNA synthesis in rat primary hepatocyte cultures. The PP nafenopin induced a 2.3-fold increase in DNA synthesis but there was no further increase upon co-administration of either TNFα or a suboptimal concentration of EGF. Furthermore, there was no gross dysregulation of the CDK and cyclin protein expression profile upon stimulation with nafenopin. Using a specific epidermal growth factor receptor tyrosine kinase inhibitor (4-(3-chloro-4-fluorophenylamino)-7-methoxy-6-(3-[1-pyrolidino])-propoxyquinazoline, EGFR-TKI), we show that signalling through EGF-R is not required for nafenopin-induced DNA synthesis. The EGFR-TKI also prevented progression into S phase upon stimulation with TNFα, but DNA synthesis was not reduced to control levels, indicating that TNFα has a mitogenic activity in the absence of EGF signalling. Therefore, although TNFα can act as a priming factor for growth factors such as EGF, nafenopin does not appear to act via this mechanism." @default.
• W2186803608 created "2016-06-24" @default.
• W2186803608 creator A5046722857 @default.
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• W2186803608 date "1999-12-15" @default.
• W2186803608 modified "2023-10-12" @default.
• W2186803608 title "Induction of DNA replication by peroxisome proliferators is independent of both tumour necrosis factor α priming and EGF-receptor tyrosine kinase activity" @default.
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• W2186803608 doi "https://doi.org/10.1242/jcs.112.24.4785" @default.
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