<原著>アンジオテンシンIIのラット血管平滑筋細胞肥大作用 : c-mycアンチセンス オリゴデオキシヌクレオチドを用いた実験的研究
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The study investigated whether the expression of mRNA for c-myc is essential in VSMC hypertrophy induced by Angiotensin II (Ang.II) and explored the possibilty of inhibiting their growth using antisense oligodeoxynucleotides (ODN) for c-myc mRNA. We used antisense ODN specific for c-myc mRNA from exon 2 (1015-1029). Cultured vascular smooth muscle cells (VSMC) were isolated from the thoracic aorta of Sprague-Dawley rats (male, 7-8 weeks) by the explant method. These cells (passage 4-7) were brought to the subconfluent state, and then the medium was changed to a low serum concentration. After 48 hours, the VSMC were stimulated by 10^<-5> M Ang. II with or without antisense ODN. Ang. II increased the uptake of [^3H]thymidine and [^3H]leucine by the VSMC. After 5 days, the cell number was constant. Ang. II increased [^3H]thymidine uptake to VSMC, which was specifically inhibited by antisense ODN for c-myc mRNA in a dose-dependent manner. More than 5 pM of antisense ODN produced significant inhibition, and a maximal inhibitory effect of 75% at a concentration of 500 pM. However, sense ODN did not have any effect. The addition of c-myc antisense ODN 6 hours after Ang. II stimulation did not decrease [^3H]thymidine uptake into VSMC, because c-myc was an immediate early response gene induced by Ang. II stimulation. Similarly, c-myc antisense ODN decreased the [^3H]leucine uptake into VSMC induced by Ang. II. These results indicate that c-myc is necessary for VSMC hypertrophy induced by Ang. II, using antisense ODN to inhibit specific gene expression.
- 近畿大学の論文
- 1995-06-25
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