Objective      To study the effect of adenine nucleotide translocase 1 (ANT1) gene over-expression on apoptosis of vascular smooth muscle cells (VSMC) in a rat carotid balloon injury model induced by adenovirus plasmid.       Methods      Seventy-two SD rats were randomly divided into normal group

non-transfection group

Ad-GFP transfection group and Ad-ANT1 transfection group (18 in each group). ANT1 gene was transfected into rat carotid arteries with Ad-ANT1 adenovirus after a rat carotid balloon injury model was established. The arteries were harvested on days 7

14 and 28 after operation. Expression of ANT-1

BAX

and Bcl-2 in arteries was detected by RT-PCR

Western blotting

and immunohistochemistry

respectively

with HE staining. Apoptosis of VSMC in tunica intima and tunica media of the model was assayed with TUNEL staining.       Results      The ANT1 gene was significantly expressed in rat carotid arteries after Ad-ANT1 transfection and reached its peak level on day 14

which was significantly higher in Ad-ANT1 transfection group than in Ad-GFP transfection group and balloon injury group（P0.01）. The expression level of BAX was significantly higher in Ad-ANT1 transfection group than in Ad-GFP transfection group and balloon injury group on days 7 and 14 after transfection（P0.05）. The expression level of Bcl-2 was higher in Ad-ANT1 transfection group than in normal group（P0.05）. However

no significant difference was found in expression level of Bcl-2 between the two groups（P0.05）.The apoptosis rate of VSMC in tunica intima and tunica media of the model was significantly higher in Ad-ANT1 transfection group than in the other 3 groups（P0.05）. The tunica intima/ tunica media area ratio in the model was lower in Ad-ANT1 transfection group than in Ad-GFP transfection group and balloon injury group on days 14 and 28 after transfection（P0.05）.       Conclusion      Adenovirus plasmid-induced over-expression of ANT1 gene induces apoptosis of VSMC in tunica intima/ tunica media of the model by up-regulating the expression of BAX.