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Abstract
Expression of the human coagulation factor VII (FVII) gene by hepatoma cells was modulated in concert with levels of glucose and insulin in the culture medium. In low glucose medium without insulin, amounts of both FVII mRNA and secreted FVII protein were coordinately increased; in the presence of glucose with insulin, both were decreased. Analysis of the FVII promoter showed that these effects could be reproduced in a reporter-gene system, and a small promoter element immediately upstream of the translation start site of the gene, which mediated these effects, was identified. Mutation of this element largely abrogated the glucose/insulin-responsive change in expression of the reporter gene. Several members of the CCAAT/enhancer-binding protein family were found to be capable of binding the identified sequence element but not the mutated element. The expression of a FVII minigene directed by a segment of the native FVII promoter responded to co-expressed activating and inhibiting forms of CCAAT/enhancer-binding protein beta.
Highlights
Expression of the human coagulation factor VII (FVII) gene by hepatoma cells was modulated in concert with levels of glucose and insulin in the culture medium
When cells were maintained in glucose-free basal medium supplemented with dialyzed serum, the amount of FVII:Ag secreted by the cells over a 24-h time course was significantly increased
The data presented here indicate that expression of the FVII gene can be directly modulated by fluctuations in glucose/insulin availability
Summary
Expression of the human coagulation factor VII (FVII) gene by hepatoma cells was modulated in concert with levels of glucose and insulin in the culture medium. A functional region of the FVII minimal promoter capable of interaction with C/EBP isoforms was identified and found to participate in mediating the changes in reporter gene expression attributable to fluctuations in glucose and insulin levels.
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