IFN-γ facilitates NGF-induced neuronal differentiation in PC12 cells

Natural or recombinant murine interferon-γ causes a reversible arrest of proliferation of PC12 cells. Treatment with other antimitotics (AraC, colchicine, mitomycin C, hydroxy-urea) or removal of serum, on the contrary, leads to mitotic arrest followed by cell death. IFN-γ-treated PC12 cells respond more rapidly to NGF in terms of speed of neuronal outgrowth. On the other hand, NGF potentiates the action of IFN-γ in stimulating the enzyme 2′,5′-A synthetase which shifts from an average of 4.4-fold stimulation at 48 h with IFN-γ alone to increments varying between 5- and 18-fold when PC12 cells are treated for 48 h with IFN-γ and NGF. NGF alone, on the contrary, does not exert any detectable effect on this enzyme. From these findings we propose the use of a combined treatment of PC12 cells with NGF and IFN-γ for a more rapid induction of neuronal differentiation.