Hirano F, Tanaka H, Makino Y, Okamoto K, Inaba M, Miura T, Makino I
Second Department of Internal Medicine, Asahikawa Medical College, Japan.
Biochem Biophys Res Commun. 1995 Mar 28;208(3):935-42. doi: 10.1006/bbrc.1995.1424.
We investigated the effect of bile acids on major histocompatibility complex (MHC) class I gene expression in the cultured human hepatoma cell HepG2. Not only chenodeoxycholic acid, but its stereoisomer ursodeoxycholic acid as well, increased steady state level of MHC class I mRNA. When various bile acids were studied, inducibility of MHC class I mRNA was closely associated with the hydrophobicity of the corresponding bile acids. Pretreatment of the cells with a protein kinase C (PKC) inhibitor H7 suppressed induction of MHC class I mRNA by those bile acids. Furthermore, treatment of the cells with chenodeoxycholic acid significantly induced translocation of PKC from cytosol to membrane. In summary, our data strongly indicate up-regulatory effect of bile acids on MHC class I mRNA expression, most probably via activation of PKC-dependent pathway.
我们研究了胆汁酸对培养的人肝癌细胞HepG2中主要组织相容性复合体(MHC)I类基因表达的影响。不仅鹅去氧胆酸,而且其立体异构体熊去氧胆酸也能提高MHC I类mRNA的稳态水平。当研究各种胆汁酸时,MHC I类mRNA的诱导性与相应胆汁酸的疏水性密切相关。用蛋白激酶C(PKC)抑制剂H7预处理细胞可抑制这些胆汁酸对MHC I类mRNA的诱导。此外,用鹅去氧胆酸处理细胞可显著诱导PKC从细胞质向细胞膜的转位。总之,我们的数据有力地表明胆汁酸对MHC I类mRNA表达具有上调作用,很可能是通过激活PKC依赖性途径实现的。