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| 題名: | Interleukin-1-beta gene, but not the interleukin-1 receptor antagonist gene, is associated with Graves' disease |
| 作者: | Chen, RH;Chen, WC;Chang, CT;Tsai, CH;Tsai, FJ |
| 貢獻者: | 附設醫院內科部;China Med Univ, China Med Univ Hosp, Dept Med, Taichung, Taiwan;China Med Univ, China Med Univ Hosp, Dept Urol, Taichung, Taiwan;China Med Univ, China Med Univ Hosp, Dept Med Genet, Taichung, Taiwan;China Med Univ, China Med Univ Hosp, Dept Pediat, Taichung, Taiwan;Taichung Healthcare & Management Univ, Taichung, Taiwan |
| 日期: | 2005 |
| 上傳時間: | 2010-09-24 14:18:56 (UTC+8) |
| 出版者: | WILEY-LISS |
| 摘要: | The pathological mechanism of restenosis is primarily attributed to excessive proliferation of vascular smooth muscle cells (SMC). Actinomycin D has been regarded as a potential candidate to prevent balloon injury-induced neointimal formation. To explore its molecular mechanism in regulating cell proliferation, we first showed that actinomycin D markedly reduced the SMC proliferation via the inhibition of BrdU incorporation at 80 nM. This was further supported by the G1-phase arrest using a flowcytometric analysis. Actinomycin D was extremely potent with an inhibitory concentration IC50 at 0.4 nM, whereas the lethal dose LD50 was at 260 mu M. In an in vivo study, the pluronic gel containing 80 nM and 80 lMactinomycin D was applied topically to surround the rat carotid adventitia; the thickness of neointima was substantially reduced (45 and 55%, respectively). The protein expression levels of proliferating cell nuclear antigen ( PCNA), focal adhesion kinase (FAK), and Raf were all suppressed by actinomycin D. Extracellular signal-regulated kinases (Erk) involved in cell-cycle arrest were found to increase by actinomycin D. These observations provide a detailed mechanism of actinomycin D in preventing cell proliferation thus as a potential intervention for restenosis. |
| 關聯: | JOURNAL OF CLINICAL LABORATORY ANALYSIS 19(4):133-138 |
| 顯示於類別: | [台中附設醫院] 期刊論文
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