Abstract
Murine C127 fibroblasts carrying an expression vector for a human interferon gene (HuIFN-beta, under the control of a constitutive promoter) can be induced to produce murine (Mu) IFN by double-stranded (ds) RNA or virus infection. Fibroblasts treated with the protein kinase C activators 1-oleyl-2-acetylglycerol (OAG) or phorbol-12-myristate-13-acetate (PMA) secrete greater amounts of MuIFN than untreated cells, but the same amount of HuIFN-beta. Accordingly, the level of MuIFN-beta mRNA increases in the presence of protein kinase C activators whereas that of HuIFN-beta mRNA is unchanged. In time course experiments after induction with dsRNA, accumulation of MuIFN-beta mRNA is observed within 30 min in the presence of OAG, when this mRNA cannot be detected in control cells. The protein kinase C activators increase accumulation of MuIFN-beta mRNA, even in the presence of the inhibitor of protein synthesis cycloheximide. A similar increase in MuIFN-beta mRNA is observed in C243 fibroblasts treated with phorbol-12-myristate-13-acetate, but not in parental C127 cells. These findings suggest that protein kinase C does not promote synthesis of regulatory factors controlling transcription of IFN mRNA, but that it may be directly or indirectly involved in activation of such factors in some murine cell lines.
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