RNA synthesis inhibition stabilises urokinase mRNA in macrophages

Abstract

Urokinase-type plasminogen activator (uPA) mRNA is induced in macrophages by the lineage specific growth factor CSF-1. Upon removal of CSF-1 from bone marrow-derived macrophages (BMM), uPA mRNA decayed with a half-life of 2 h. If RNA synthesis inhibitors actinomycin D, 5,6-dichloro-1-beta-ribofuranosyl benzimidazole (DRB) or alpha-amanitin were added at the time as CSF-1 removal, the uPA message was stabilised. This was not a general effect on CSF-1 responsive mRNAs, as c-myc mRNA decayed with normal kinetics in the presence of inhibitors. The requirement for ongoing RNA synthesis for the degradation of uPA mRNA in BMM suggests that a component of the degradative pathway may be induced following removal of CSF-1.