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Background —Although loss of activity of an antioncogene, thep53 tumor suppressor gene product, has been postulated in the pathogenesis of human restenosis, little is known about the role ofp53 in the regulation of vascular smooth muscle cell (VSMC) growth. In this study, to clarify the role ofp53 in the pathogenesis of restenosis, we examined transfection of antisensep53 oligodeoxynucleotides (ODN) into VSMC in vitro and rat carotid artery in vivo.Methods and Results —The specificity of antisensep53 ODN was confirmed by a significant decrease inp53 protein. Transfection of antisensep53 ODN into VSMC resulted in a significant increase in DNA synthesis and cell number as compared with sense and scrambled ODN (P &lt;0.01). Importantly, transfection of antisensep53 ODN into rat intact carotid artery resulted in a significant increase in the ratio of neointima to medial area at 2 and 4 weeks after transfection, accompanied by a significant decrease inp53 protein (P &lt;0.01). Moreover, cotransfection of wild-typep53 plasmid completely abolished neointimal formation induced by antisensep53 ODN. The sustained effect of a single antisense ODN administration was confirmed by the kinetics of ODN in the vessel wall with the use of FITC-labeled ODN.Conclusions —Overall, the present study demonstrated that loss ofp53 by antisensep53 ODN resulted in an abnormal VSMC growth in vitro and in vivo. These results demonstrated the potential contribution ofp53 to the pathogenesis of restenosis.

circulation

Transfection of Antisense <i>p53</i> Tumor Suppressor Gene Oligodeoxynucleotides Into Rat Carotid Artery Results in Abnormal Growth of Vascular Smooth Muscle Cells

Transfection of Antisense p53 Tumor Suppressor Gene Oligodeoxynucleotides Into Rat Carotid Artery Results in Abnormal Growth of Vascular Smooth Muscle Cells