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研究生(外文):Wen-Gia Fan
論文名稱(外文):Effects of LDL on Leukocyte- or Platelet- Endothelium Interaction
指導教授(外文):Hsiun-ing Chen
外文關鍵詞:endothelial cellLDLatherosclerosis
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我們的結果顯示1)HUVECs在受到高濃度(1.4mg/ml)的低密度脂蛋白作用後,內皮細胞的型態會改變。2) 受到低密度脂蛋白作用後的HUVECs,在經過我們所測試的各個剪力強度下,白血球黏著的情形都明顯高於控制組;而其中單核球黏著又更為明顯,但是對多形性白血球卻沒有影響。3) 單核球較多形性白血球容易黏著上內皮。4)低密度脂蛋白也會使得HUVECs 的黏著分子P-selectin、 VCAM-1表現量增加。我們得到的結論為:低密度脂蛋白的作用會使得白血球(尤其是單核球)的黏著情形增加,而P-selectin、VCAM-1的表現或許參與了此反應。
Atherosclerosis is a chronic inflammatory disease. Previous studies have indicated that abnormally elevated concentrations of plasma LDL will result in an increase in rolling/adhesion of leukocyte and the expression of the relevant adhesion molecules. The existing evidence suggests that the treatment of native LDL (nLDL) in cultured human vascular endothelial cells will induce calcium transient and trigger vascular cell adhesion molecule-1 (VCAM-1) and E-selectin expression. However, the role of nLDL in the interaction of leukocytes/platelets and endothelial cells is largely unknown. To investigate whether the endothelium- leukocyte or platelet interactions could be altered by nLDL, cultured human umbilical vein endothelial cells (HUVECs) were treated with nLDL. Leukocyte and platelet adhesion to HUVECs was subsequently measured by using a tapered flow chamber that has a linear variation of shear stress across its flow channel. To verify which adhesion molecules are involved, the immunostaining were executed. Our data showed that 1) the pretreatment of high dose of nLDL (1.4mg/ml) would change cell morphology of HUVECs; 2) leukocytes, especially monocyte, but not neutrophil , adhered more readily to nLDL-treated HUVECs than to the control group at all shear stress levels tested; 3) the adhesiveness of monocyte on endothelium was higher than that of neutrophil; 4) the expression of P-selectin and VCAM-1 in HUVECs increased after nLDL pretreatment. We conclude that nLDL pretreatment enhances leukocytes adhesiveness, especially monocyte, and that P-selectin and VCAM-1 may be involved.
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參考文獻 ----------------------------56
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