LIPOPROTEIN (A), COAGULATION AND FIBRINOLYSIS

脂蛋白（a）（Lp（a））是一种低密度脂蛋白。 高 Lp（a）水平与动脉粥样硬化性疾病高度相关 但其机制尚不清楚。 这是一个假设 应用程序，部分，这可能是由于疾病， Lp（a）水平升高诱导的纤溶系统。 本实验室的初步研究表明，Lp（a）是一种 纤溶酶原激活的竞争性抑制剂，Lp（a）结合 与一种纤溶酶原激活剂的结合，Lp（a）阻断了 纤溶酶原与其受体的相互作用， 高Lp（a）水平的患者， 载脂蛋白（a）则有不同的分布模式。 提出要 系统研究：1）脂蛋白（a）对纤溶酶原的影响 链激酶-纤溶酶复合物催化活化，尿激酶 和组织纤溶酶原激活剂; 2）Lp（a）水平对 纤溶酶原与内皮细胞和单核细胞样（U-937）的结合 Lp（a）对纤溶酶原相互作用的影响 纤维蛋白。 作为这些研究的一部分， 此外，亦会研究载脂蛋白（a）与这些细胞的关系。 Lp（a）的作用 对组织型纤溶酶原激活剂与内皮细胞结合的影响 还将检查纤维蛋白。

Lipoprotein (a) (Lp(a) is a form of low density lipoprotein. High levels of Lp(a) are highly correlated with atherosclerotic diseAse but the mechanism is unknown. It is the hypothesis of this application that, in part, this may be attributed to disorders in the fibrinolytic system induced by increased levels of Lp(a). Preliminary studies in this laboratory indicate that Lp(a) is a competitive inhibitor of plasminogen activation, that Lp(a) binds to one type of plasminogen activator, that Lp(a) blocks the binding of plasminogen to its receptor and that in normal subjects and patients with high Lp(a) levels the subunit molecular weight for apo(a) has a different distribution pattern. It is proposed to systematically study: 1) the effect of Lp(a) on plasminogen activation catalyzed by streptokinase-plasmin complexes, urokinase and tissue plasminogen activator; 2) the effect of Lp(a) levels on the binding of plasminogen to endothelial and monocyte-like (U-937) cells; 3) the effect of Lp(a) on the interaction of plasminogen with fibrin. As part of these studies, the direct binding of apo(a) with these cells will also be studied. The effect of Lp(a) on the binding of tissue plasminogen activator to endothelial cells and fibrin will also be examined.