Lipopolysaccharide signaling induces serum amyloid A (SAA) synthesis in human hepatocytes in vitro
K Migita, S Abiru, M Nakamura, A Komori… - FEBS …, 2004 - Wiley Online Library
K Migita, S Abiru, M Nakamura, A Komori, Y Yoshida, T Yokoyama, M Daikoku, T Ueki…
FEBS letters, 2004•Wiley Online LibraryTo investigate the role of lipopolysaccharide (LPS) in hepatocyte activation, we examined
the expression of Toll‐like receptor 4 (TLR4), the putative receptor for LPS in human
hepatocytes. TLR4 mRNA and protein expression was confirmed in human hepatocytes.
Stimulation of human hepatocytes with LPS results in rapid degradation of IkappaB‐α and
mitogen activated protein kinase activation. Human hepatocytes stimulated by LPS
produced serum amyloid A protein. Our data suggest that human hepatocytes utilize …
the expression of Toll‐like receptor 4 (TLR4), the putative receptor for LPS in human
hepatocytes. TLR4 mRNA and protein expression was confirmed in human hepatocytes.
Stimulation of human hepatocytes with LPS results in rapid degradation of IkappaB‐α and
mitogen activated protein kinase activation. Human hepatocytes stimulated by LPS
produced serum amyloid A protein. Our data suggest that human hepatocytes utilize …
To investigate the role of lipopolysaccharide (LPS) in hepatocyte activation, we examined the expression of Toll‐like receptor 4 (TLR4), the putative receptor for LPS in human hepatocytes. TLR4 mRNA and protein expression was confirmed in human hepatocytes. Stimulation of human hepatocytes with LPS results in rapid degradation of IkappaB‐α and mitogen activated protein kinase activation. Human hepatocytes stimulated by LPS produced serum amyloid A protein. Our data suggest that human hepatocytes utilize components of TLR4 signal transduction pathways in response to LPS and these direct LPS‐mediated effects on hepatocytes may contribute to liver inflammation and injury.
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