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Smooth muscle cells (SMCs), before migration and proliferation in the intima of the vessel wall, change from a normal contractile to a pathological proliferating phenotype. The molecular regulatory mechanisms implicated in such phenotypic changes remain poorly understood. In this study, using differential display, we have isolated for the first time a new gene (2A3-2) that is overexpressed in a rapidly proliferating, but not synthetic, rat SMC line. This was further confirmed by northern blot performed on the 2 cell types. Moreover, balloon catheter injury of rat carotids showed, by a virtual northern technique, an upregulation of this new gene in hyperplasia vessels. This new gene (2A3-2, 1.2 kb) was present in skeletal muscle, heart, aorta, lung, liver, kidney, and spleen. In addition, 5' rapid amplification of cDNA ends (5' RACE) allowed the cloning and sequencing of this 1.2-kb gene. Comparison of this newly identified gene sequence with data banks showed a strong homology to human and bovine mitochondrial translational elongation factor. The 2A3-2 gene, identified in this study, may play a vital role in the cascade of events implicated in switching SMC phenotype from a quiescent to a proliferate one.

arteriosclerosis, thrombosis, and vascular biology

Identification and Cloning of a New Gene (2A3-2), Homologous to Human Translational Elongation Factor, Upregulated in a Proliferating Rat Smooth Muscle Cell Line and in Carotid Hyperplasia