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| 題名: | The profile of cardiac cytochrome c oxidase (COX) expression in an accelerated cardiac hypertrophy model in rats. |
| 作者: | 郭薇雯(Wei-Wen Kuo);(Chu, Chia-Yih);(Wu, Chieh-His);林子恩(Lin, Tzu-En);(Liu, Jer-Yuh);(Hsieh, Yi-Hsien);(Chu, Chu-Hsien);(Lin, Ding-Yu);(Hsu, Hsi-Hsien);黃志揚(Chih-Yang Huang)* |
| 貢獻者: | 生命科學院生物科技學系 |
| 關鍵詞: | cytochrome c oxidase (COX);complete coarctation;cardiac hypertrophy;genetically hypertensive rats |
| 日期: | 2005 |
| 上傳時間: | 2009-08-19 16:57:03 (UTC+8) |
| 摘要: | The contribution of the mitochondrial components, the main source of energy for the cardiac hypertrophic growth induced by pressure overload, is not well understood. In the present study, complete coarctation of abdominal aorta was used to induce the rapid development of cardiac hypertrophy in rats. One to two days after surgery, we observed significantly higher blood pressure and cardiac hypertrophy, which remained constantly high afterwards. We found an early increased level of cytochrome c oxidase (COX) mRNA determined by in-situ hybridization and dot blotting assays in the hypertrophied hearts, and a drop to the baseline 20 days after surgery. Similarly, mitochondrial COX protein level and enzyme activity increased and, however, dropped even lower than baseline 20 days following surgery. In addition, in natural hypertension-induced hypertrophic hearts in genetically hypertensive rats, the COX protein was significantly lower than in normotensive rats. Taken together, the lower efficiency of mitochondrial activity in the enlarged hearts of long-term complete coarcted rats or genetically hypertensive rats could be, at least partially, the cause of hypertensive cardiac disease. Additionally, the rapid complete coarctation-induced cardiac hypertrophy was accompanied by a disproportionate COX activity increase, which was suggested to maintain the cardiac energy-producing capacity in overloaded hearts. |
| 關聯: | JOURNAL OF BIOMEDICAL SCIENCE12(4):601~610 |
| 顯示於類別: | [生物科技學系暨碩士班] 期刊論文
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