Weigel P H, Frost S J, McGary C T, LeBoeuf R D
Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston.
Int J Tissue React. 1988;10(6):355-65.
We have previously hypothesized that hyaluronic acid (HA) and fibrin specifically interact and help orchestrate the early stages of the inflammatory response and wound healing (J. Theoretic. Biol. 119, 219, 1986). In the present work we have extended studies to confirm this prediction. Several approaches were used to show that human fibrinogen specifically binds to hyaluronic acid. In addition, this latter glycosaminoglycan greatly stimulated the in vitro formation of fibrin clots induced by thrombin. The presence of hyaluronic acid also altered the structure of the final fibrin gel. Removal of circulating hyaluronic acid in blood is therefore probably vital in order to maintain normal haemostasis. Evidence is presented to suggest that an endocytic receptor recycling process is responsible for the ability of liver endothelial cells to perform this function and remove HA from the blood. Although hyaluronic acid levels are initially low in a blood clot, the proposed wound-healing model explains why and how HA levels increase and the functional and structural significance of this polysaccharide during wound healing.
我们之前曾提出假设，即透明质酸（HA）和纤维蛋白会发生特异性相互作用，并有助于协调炎症反应和伤口愈合的早期阶段（《理论生物学杂志》119卷，219页，1986年）。在本研究中，我们扩展了研究以证实这一预测。我们采用了多种方法来证明人纤维蛋白原能特异性结合透明质酸。此外，后一种糖胺聚糖极大地刺激了凝血酶诱导的纤维蛋白凝块的体外形成。透明质酸的存在也改变了最终纤维蛋白凝胶的结构。因此，为维持正常止血，去除血液中循环的透明质酸可能至关重要。有证据表明，一种内吞受体循环过程负责肝内皮细胞执行此功能并从血液中清除HA的能力。尽管血凝块中透明质酸水平最初较低，但所提出的伤口愈合模型解释了HA水平升高的原因和方式，以及这种多糖在伤口愈合过程中的功能和结构意义。
