Response to iron overload in cultured hepatocytes.

ABSTRACT: Iron is essential for a variety of physiological processes. Hepatic iron overload acts as a trigger for the progression of hepatic steatosis to nonalcoholic steatohepatitis and hepatocellular carcinoma. In the present study, we aimed to study the effects of iron overload on cellular responses in hepatocytes. Rat primary hepatocytes (RPH), mouse primary hepatocytes (MPH), HepG2 human hepatoma cells and Hepa1-6 mouse hepatoma cells were treated with FeCl₃. Treatment with FeCl₃ effectively increased iron accumulation in primary hepatocytes. Expression levels of molecules involved in cellular signaling such as AMPK pathway, TGF-β family pathway, and MAP kinase pathway were decreased by FeCl₃ treatment in RPH. Cell viability in response to FeCl₃ treat

SUBMITTER: Chen HJ 

PROVIDER: S-EPMC7713074 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature