Basic fibroblast growth factor uniquely stimulates quiescent vascular smooth muscle cells and induces proliferation and dedifferentiation.

Blood vessels normally remain stable over the long term. However, in atherosclerosis, vascular cells leave the quiescent state and enter an activated state. Here, we investigated the factors that trigger the breakage of the quiescent state by screening growth factors and cytokines using a vascular smooth muscle cell (SMC) line and an endothelial cell (EC) line. Despite known functions of the tested factors, only basic fibroblast growth factor (bFGF) was identified as a potent trigger of quiescence breakage in SMCs, but not ECs. bFGF disrupted tight SMC-monolayers and caused morphological changes, proliferation, and dedifferentiation. Human primary SMCs, but not ECs, also showed similar results. Aberrant SMC proliferation is a critical histological event in atherosclerosis. We, thus, provide further insights into the role of bFGF in vascular pathobiology.