RESUMEN
AIM: The present study is to investigate the inhibitory effect of the transfer of replication-defective retroviral recombinant plasmid encoding a wild-type P16 ink4a gene on the formation of restenosis after rabbit carotid arterial injury in vivo.METHODS:A replication-defective retroviral recombinant plasmid encoding wild-type gene P16 ink4a was constructed and the packaged high titer virus stock was obtained. It was transferred into the rabbit carotid arterial wall immediately after injury. The P16 ink4a mRNA expression in the arteries was examined by Northern blot and in situ hybridization. The effect of overexpression of the P16 ink4a gene on arterial intima hyperplasia was determined by pathophysiological method. RESULTS: The exogenous P16 ink4a could be effectively transferred into injured arterial wall by retroviral recombinant plasmid and the gene products could inhibit smooth muscle cells proliferation (11.80?3.54 vs 25.20?5.12,P