Hojima Y, Cochrane C G, Wiggins R C, Austen K F, Stevens R L
Blood. 1984 Jun;63(6):1453-9.
A large number of negatively charged macromolecules, including DNA, glycosaminoglycans, and proteoglycans, were tested as possible activators of the contact (Hageman factor) system in vitro. Activation was assessed by conversion of prekallikrein to kallikrein, as determined by amidolytic assay and by cleavage of 125I-Hageman factor into 52,000- and 28,000-dalton fragments. Of particular interest to these studies, heparin proteoglycan and glycosaminoglycan from rat peritoneal mast cells, and squid chondroitin sulfate E, which is representative of the glycosaminoglycan from cultured mouse bone marrow derived mast cells, induced the reciprocal activation between Hageman factor and prekallikrein. In addition, naturally occurring heparin glycosaminoglycans from pig mucosa, bovine lung, and rat mast cells also induced activation. In contrast, native connective tissue matrix glycosaminoglycans and proteoglycans from several sources were inactive, although when one such chondroitin sulfate was further sulfated in vitro, it gained activity. When the negative charge of the activating agents was blocked by the addition of hexadimethrine bromide, the cleavage of 125I-Hageman factor in the presence of prekallikrein was prevented. The active negatively charged macromolecules induced cleavage of 125I-high molecular weight kininogen in normal plasma but not in Hageman factor-deficient or prekallikrein-deficient plasmas. Reconstitution of prekallikrein-deficient plasma with purified prekallikrein restored the kininogen cleavage upon addition of the active proteoglycans. These results suggest that both heparin from connective tissue mast cells and highly sulfated chondroitin sulfate E from cultured mouse bone marrow derived mast cells (which are considered synonomous with mucosal mast cells) could activate the contact system of plasma subsequent to an activation secretion response.
大量带负电荷的大分子,包括DNA、糖胺聚糖和蛋白聚糖,在体外作为接触(Hageman因子)系统的可能激活剂进行了测试。通过酰胺水解测定法测定前激肽释放酶转化为激肽释放酶,并通过将125I-Hageman因子裂解为52,000道尔顿和28,000道尔顿的片段来评估激活情况。在这些研究中特别有趣的是,来自大鼠腹膜肥大细胞的肝素蛋白聚糖和糖胺聚糖,以及来自培养的小鼠骨髓来源肥大细胞的糖胺聚糖的代表鱿鱼硫酸软骨素E,诱导了Hageman因子和前激肽释放酶之间的相互激活。此外,来自猪黏膜、牛肺和大鼠肥大细胞的天然肝素糖胺聚糖也诱导了激活。相比之下,来自多个来源的天然结缔组织基质糖胺聚糖和蛋白聚糖没有活性,尽管当一种这样的硫酸软骨素在体外进一步硫酸化时,它获得了活性。当通过添加溴化己二甲铵阻断激活剂的负电荷时,在存在前激肽释放酶的情况下125I-Hageman因子的裂解被阻止。活性带负电荷的大分子在正常血浆中诱导125I-高分子量激肽原的裂解,但在Hageman因子缺乏或前激肽释放酶缺乏的血浆中则不诱导。用纯化的前激肽释放酶重建前激肽释放酶缺乏的血浆,在添加活性蛋白聚糖后恢复了激肽原的裂解。这些结果表明,来自结缔组织肥大细胞的肝素和来自培养的小鼠骨髓来源肥大细胞(被认为与黏膜肥大细胞同义)的高度硫酸化的硫酸软骨素E在激活分泌反应后都可以激活血浆的接触系统。