Janoff A, Feinstein G, Malemud C J, Elias J M
J Clin Invest. 1976 Mar;57(3):615-24. doi: 10.1172/JCI108317.
The present work was undertaken to explore the effect of two purified neutral proteases derived from human peripheral blood polymorphonuclear leukocytes (PMN) on articular cartilage as a model of joint injury. Human leukocyte elastase and chymotrypsin-like enzyme, purified by affinity chromatography, released 32SO4 from labeled rabbit articular cartilage slices in vitro. Release of isotope was initially delayed, suggesting that either a lag in enzyme penetration occurs or that size of degradation fragments is a limiting factor in diffusion of label out of the tissue. The release of 35SO4 was inhibited by preincubation of elastase and chymotrypsin-like enzyme with human alpha 1-anti-trypsin, or with their specific chloromethyl ketone inactivators, and the action of elastase was also inhibited by a monospecific antiserum to PMN elastase, freed of major serum proteinase inhibitors. Immunohistochemical staining procedures revealed the presence of PMN elastase inside the matrix of cartilage slices after a 20-min exposure of tissue to either the pure enzyme or crude PMN granule extract. Serum alpha 1-antitrypsin failed to penetrate into the cartilage slices under identical in vitro conditions. In association with the results reported in the accompanying paper, these findings suggest a model of cartilage matrix degradation by PMN neutral proteases in which local protease-antiprotease imbalance, coupled with different rates of penetration of protease and antiprotease into target tissue, plays a key role in accounting for matrix damage.
本研究旨在探讨源自人外周血多形核白细胞(PMN)的两种纯化中性蛋白酶对关节损伤模型关节软骨的影响。通过亲和层析纯化的人白细胞弹性蛋白酶和类胰凝乳蛋白酶在体外从标记的兔关节软骨切片中释放出32SO4。同位素的释放最初有延迟,这表明要么是酶渗透存在滞后,要么是降解片段的大小是标记物从组织中扩散的限制因素。弹性蛋白酶和类胰凝乳蛋白酶与人α1-抗胰蛋白酶或其特异性氯甲基酮灭活剂预孵育可抑制35SO4的释放,并且去除主要血清蛋白酶抑制剂的PMN弹性蛋白酶单特异性抗血清也可抑制弹性蛋白酶的作用。免疫组织化学染色程序显示,在将组织暴露于纯酶或粗制PMN颗粒提取物20分钟后,软骨切片基质内存在PMN弹性蛋白酶。在相同的体外条件下,血清α1-抗胰蛋白酶未能渗透到软骨切片中。结合随附论文中报道的结果,这些发现提示了一种PMN中性蛋白酶降解软骨基质的模型,其中局部蛋白酶-抗蛋白酶失衡,以及蛋白酶和抗蛋白酶进入靶组织的不同速率,在解释基质损伤中起关键作用。