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| 題名: | Detection of severe acute respiratory syndrome-associated coronavirus in pneumocytes of the lung |
| 作者: | Chow, KC;Hsiao, CH;Lin, TY;Chen, CL;Chiou, SH |
| 貢獻者: | 附設醫院醫研部;Natl Chung Hsing Univ, Inst Biomed Sci, Taichung 40227, Taiwan;Natl Chung Hsing Univ, Grad Inst Vet Microbiol, Taichung 40227, Taiwan;Natl Taiwan Univ Hosp, Dept Pathol, Taipei 100, Taiwan;China Med Univ Hosp, Dept Pathol, Taichung, Taiwan;China Med Univ Hosp, Dept Med Res, Taichung, Taiwan |
| 日期: | 2004 |
| 上傳時間: | 2010-09-24 15:00:22 (UTC+8) |
| 出版者: | AMER SOC CLINICAL PATHOLOGY |
| 摘要: | The pharmacological mechanisms of a synthetic compound 1-benzyl-3-(5'-hydroxymethyl-2'-furyl) indazole (YC-1) in preventing smooth muscle cell proliferation remains to be elucidated. The present study was aimed to explore the effects of YC-1 on certain molecules responsible for cell proliferation, including transforming growth factor (TGF)-beta1, soluble guanylyl cyclase (sGC) and focal adhesion kinase (FAK). The in vivo assay was correlated to the in vitro results of YC-1 on vascular stenosis. YC-1 was applied topically via a pluronic gel onto the balloon-injured rat carotid arteries, which were then harvested two weeks later for histological analysis. Our in vitro results showed that TGF-beta1 was suppressed by YC-1 by 50%. The translational level of sGC was threefold activated by YC-1 while the transcription level of sGC was increased up to 24-fold. FAK, the molecule responsible for cell proliferation and migration, was suppressed by YC-1 on the translational levels for 72%. These in vitro results were in consistent with the in vivo observation that the area ratio of neointima to media was reduced by YC-1. This study provides insights into the pharmacological mechanisms of YC-1 in preventing abnormal smooth muscle cell proliferation and thus supports the use of YC-1 as an adjuvant therapy for balloon injury-induced restenosis. |
| 關聯: | AMERICAN JOURNAL OF CLINICAL PATHOLOGY 121(4):574-580 |
| 顯示於類別: | [台中附設醫院] 期刊論文
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