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

Smooth muscle cells (SMCs), before migration and proliferation in the intim a of the vessel wall, change from a normal contractile to a pathological pr oliferating phenotype. The molecular regulatory mechanisms implicated in su ch phenotypic changes remain poorly understood. In this study, using differ ential 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 li ne. This was further confirmed by northern blot performed on the 2 cell typ es. 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, aort a, 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 quiesce nt to a proliferate one.