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題名 | Role of Endothelial Cell Mitosis in Transendothelial Transport of Low Density Lipoprotein in Hypercholesterolemic and Normal Rabbits=在高膽固醇血症和正常兔子主動脈中內皮細胞分裂於穿內皮細胞層低密度脂蛋白輸送所扮演的角色 |
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作者 | 陳玉怜; 楊元正; 李雲萍; 陳雅婷; 丁燿宗; 林幸榮; Chen, Yuh-lien; Yang, Yuan-jeng; Li, Yun-ping; Chen, Ya-ting; Ding, Yaw-zon; Lin, Shing-jong; |
期刊 | 中華醫學雜誌 |
出版日期 | 19960800 |
卷期 | 58:2 1996.08[民85.08] |
頁次 | 頁71-78 |
分類號 | 415.384 |
語文 | eng |
關鍵詞 | 動脈硬化; 內皮細胞; 細胞接合處; 低密度脂蛋白; 巨分子運輸; Atherosclerosis; Endothelial cell; Intercellular junction; Low density lipoprotein; Macromolecular transport; |
中文摘要 | 背景 動脈硬化的主要特徵為在血管壁上有區域性脂肪堆積和平滑肌 細胞增生。在動脈硬化的最初形成和進展過程中,脂蛋白類(lipoproteins)會從血 液通過動脈內皮細胞層而在血管壁堆積,因此內皮細胞對巨分子的通透性質是 造成動脈硬化的一個重要成因。目前對於脂蛋白類如何通過內皮細胞層的機制 仍不清楚,但最近一系列以大白鼠為實驗動物的研究中,證明了在分裂的內皮 細胞旁打開的細胞接合處,可當為加強巨分子通過的重要路徑,而這路徑可能 即是導致脂肪在血管內膜堆積及動脈硬化的成因。因為高膽固醇血症是動脈硬 化的一重要危險因子,所以我們想測試在高膽固醇血症時,內皮細胞週轉與穿 內皮細胞層低密度脂蛋白輸送之間的關係,以進一步了解高膽固醇血症加速形 成血管硬化的機轉。 方法 在本實驗,使用30隻雄性紐西蘭白兔,分為兩組,一為餵食高膽固醇(1%) 飼料(15隻),一為餵食正常飼料(15隻),共6週之久。血中的膽固醇,三酸甘油 脂之濃度以試劑偵測其兩組的差異性。接著使用以螢光物質Lucifer yellow (LY) 標定低密度脂蛋白為追蹤劑,打入兔子的血管內,而10分鐘後在螢光顯微鏡下 觀察兩組動物的胸主動脈內皮細胞層對LY-低密度脂蛋白的通透性,並定量分 析此通透性與內皮細胞分裂的相關性。 結果 在餵食正常飼料或餵食高膽固醇飼料的兔子,其內皮細胞分裂速率都相 當低,分別為0.0022 +/- 0.0007%和0.0004 +/- 0.0001%,而儘管其分裂速率相當 低,但68.2 +/- 8.4%和74.3 +/- 9.0%的這些分裂細胞對LY-低密度脂蛋白有通透 性。另外,65.0 +/- 9.2%和64.4 +/- 11.3%對LY-低密度脂蛋白有通透性的位置, 是有分裂細胞分佈的。 結論 這些實驗結果證明在高膽固醇血症和正常兔子中,其內皮細胞分裂與低 密度脂蛋白通過內皮細胞層有密切關係。由這些觀察,支持一理論,即內皮細 胞在更替時,其旁暫時打開的細胞接合處,能提供脂蛋白通過內皮細胞層至動 脈壁內,而導致脂肪堆積,加速形成動脈硬化。 |
英文摘要 | Background. Atherosclerosis is characterized by focal areas of lipid accumulation and intimal smooth muscle cell proliferation in large arteries. It has been suggested that the permeability of arterial endothelium to lipid is an important factor in the initiation and progression of atherosclerosis. The mechanism by which macromolecules such as low density lipoprotein (LDL) enter the arterial wall, however, is still not completely understood. Our previous studies have demonstrated that there is close association of endothelial cell turnover with transendothelial macromolecular transport in normal rat aorta. Because hypercholesterolemia has been well documented as one of the major risk factors for atherosclerosis, we explore the relationship between endothelial cell mitosis and transendothelial transport of LDL in hypercholesterolemic rabbits. Methods. The present study is designed to perform on thoracic aortae from 30 male New Zealand white rabbits fed with either 1% cholesterol-enriched diet (HC group; n = 15) or normal diet (NC group; n = 15). The concentrations of serum cholesterol and triglycerides from two groups were measured by enzymatic procedures using commercial kits. The aortae of hypercholesterolemic and normocholesterolemic rabbits underwent perfusion-fixation 10 min following the intravenous injection of low density lipoprotein conjugated with Lucifer yellow (LY-LDL) for fluorescence microscopy. En face preparations of the thoracic aortae stained with hematoxylin allowed the identification of ECs in mitosis. The relationship between LY-LDL leakage and endothelial cell mitosis was determined. Results. Although endothelial cell mitosis is infrequent (NC: 0.0022 +/- 0.0007%; HC: 0.0004 +/- 0.0001%) in the thoracic aorta of New Zealand white rabbits, 68.2 +/- 8.4% (NC) or 74.3 +/- 9.0% (HC) of dividing cells in the M phase were associated with LYLDL leakage. These dividing cells accounted for 65.0 +/- 9.2% (NC) or 64.4 +/- 11.3% (HC) of all LY-LDL leaky spots. Conclusions. Thus, this study not only confirmed the close association of EC mitosis with macromolecular permeability in normal group, but also demonstrated that the same relationship existed in hypercholesterolemic rabbits. These observations lend support to the theory that transiently open junctions surrounding the endothelial cells undergoing cell turnover provide pathways through which LDL enters the subendothelial space, resulting in lipid accumulation and atherosclerosis. |
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