First Author | Vik DP | Year | 1996 |
Journal | Scand J Immunol | Volume | 44 |
Issue | 3 | Pages | 215-22 |
PubMed ID | 8795714 | Mgi Jnum | J:35705 |
Mgi Id | MGI:83153 | Doi | 10.1046/j.1365-3083.1996.d01-299.x |
Citation | Vik DP (1996) Regulation of expression of the complement factor H gene in a murine liver cell line by interferon-gamma. Scand J Immunol 44(3):215-22 |
abstractText | Factor H is a regulatory protein of the alternative pathway of complement activation that is synthesized mainly in the liver. The authors used the +/+ Li murine liver cell line as a model for examining its regulation. When +/+ Li cells were incubated with IFN-gamma, the levels of factor H mRNA increased in a dose-dependent manner, achieving a maximal response at a concentration of 50-100 units/ml. The increase in factor H mRNA levels was paralleled by an increase in factor H secretion. The kinetics of induction of factor H mRNA were slow, with the response reaching near maximal levels at 24 h. The increase in factor H mRNA by IFN-gamma was dependent on protein synthesis, as cycloheximide abolished the response. The presence of IFN-gamma was required for the entire incubation period in order to produce a maximal response. The luciferase system was used in an attempt to identify an interferon-responsive element. Luciferase constructs containing from 807 to 236 bp of upstream sequence responded to IFN-gamma with a twofold induction of luciferase activity, whereas a construct containing 83 bp of 5' sequence did not. Thus, IFN-gamma stimulates factor H mRNA transcription through a protein intermediary that interacts with the promoter between positions -83 and -236. |