Abstract:
:Among the transcription factors critical for cell cycle regulation is the proto-oncogene c-myc. The expression of c-myc upon vascular injury and its inhibition by antisense oligodeoxynucleotides have demonstrated the importance of this protein in the control of proliferation for many cell types, including vascular smooth muscle cells. Liposomes can enhance cellular incorporation of antisense oligodeoxynucleotides, but cellular uptake of oligonucleotides in this manner is still suboptimal, and the oligonucleotides are not protected from enzymatic degradation. Physico-chemical modifications of the oligomers must be developed before antisense oligodeoxynucleotides can be considered as a potential gene therapy for many of the human diseases. This study reports on the enhanced cellular incorporation of antisense phosphodiester oligonucleotides when conjugated to lipophilic linkers. Conjugated phosphodiesters of antisense c-myc oligodeoxynucleotides inhibited cultured human aortic smooth muscle cell growth by 47.5 ± 1.0% 4 days following only a 24-h exposure to the conjugated antisense phosphodiester oligonucleotides. Liposome-enhanced, but unconjugated, phosphodiester and phosphorothioate oligonucleotides were less effective (24.4 ± 1.9% and 29.5 ± 3.1% inhibition, respectively). Smooth muscle cell growth inhibition by antisense c-myc oligodeoxynucleotides correlated with the suppression of nuclear c-myc protein expression. Thus, antisense c-myc oligodeoxynucleotides conjugated to lipid-soluble linkers enhanced cellular incorporation as well as intracellular retention of oligodeoxynucleotides, resulting in rapid and sustained inhibition of c-myc expression of smooth muscle cells. This, in turn, caused a prolonged growth inhibition compared to unconjugated oligodeoxynucleotides.
journal_name
Drug Delivjournal_title
Drug deliveryauthors
Koo EW,Edelman ERdoi
10.3109/10717549609029444subject
Has Abstractpub_date
1996-01-01 00:00:00pages
149-54issue
3eissn
1071-7544issn
1521-0464journal_volume
3pub_type
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