Basic transcription element-binding protein 2 (BTeB2) is a regulator of the proliferation and phenotypic changes of vascular smooth muscle cells (SMcs). The aim of the present study was to determine whether or not BTeB2 knockdown inhibits balloon injury-induced neointimal hyperplasia attributed to the proliferation and phenotypic changes of vascular SMcs. We found that the knockdown of BTeB2 with antisense oligonucleotides (Ad-As-BTEB2) significantly reduced the intima/media ratio compared to

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... injured arteries and vessels treated with ad-lacZ. Knockdown of BTeB2 suppresses the proliferation of cultured vascular SMcs, concurrent with the down-regulation of proliferating cell nuclear antigen, angiotensin ii type 1 receptor and plateletderived growth factor BB. in addition, BTeB2 knockdown caused the up-regulation of the differentiation marker smooth muscle α-actin and down-regulation of the dedifferentiation marker embryonic smooth muscle myosin heavy chain. The present study provides direct evidence that BTeB2 plays a critical role in balloon injury-induced neointimal hyperplasia, which is closely linked to vascular SMc proliferation and phenotypic modulation. This study highlights the fact that BTeB2 may be a potential target for the prevention of restenosis after vascular intervention.