Prevention of restenosis after PTCA by the requlation of Id, a trnscription factor of muscle differentiation.

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We examined whether the phenotypic change of vascular smooth muscle cells (VSMC) were regulated by Id protein, a helix-loop-helix type transcription without basic region. Id mRNA expression in VSMC was examined by Northern analysis using rat Id cDNA probe. Id mRNA,which was not detected in rat aortic tissue, was markedly increased in cultured VSMC from bovine and human aorta in growing phase. When cells reached confluency, Id mRNA expression was significantly reduced to 22% of growing cells. Id mRNA expression in human direct coronary atherectomy samples was also examined using reverse transcription-polymerase chain reaction. Id mRNA was detected predominantly in samples from restenotic lesion after PTCA compared to primary atherosclerotic lesion (67% vs.25%, p<0.05). VSMC growth in 5% fetal bovine serum (FBS) measured by 3H-thymidine uptake and cell number were markedly decreased by the addition of antisense oligodeoxyribo-nucleotides (ODN) to Id (30 muM) (28% and 39%, respectively, p<0.01). However, chemotactic activity of VSMC assessed by micro Boyden chamber method using 5% FCS as a chemoattractant was not reduced by Id antisense ODN.These results suggest that Id expression is closely-related to phenotype change of VSMC from contraction to proliferation but not to chemotaxis, and may suggest that the change in VSMC phenotype is transcriptionally regulated by helix-loop-helix type trans-acting factors.