OXIDATIVE AUTOACTIVATION OF LATENT COLLAGENASE BY HUMAN-NEUTROPHILS
OXIDATIVE AUTOACTIVATION OF LATENT COLLAGENASE BY HUMAN-NEUTROPHILS
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DOI：
10.1126/science.2982211
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发表时间：
1985-01-01
期刊：
影响因子：
56.9
通讯作者：
TEST, ST
中科院分区：
文献类型：
--
作者：
WEISS, SJ;PEPPIN, G;TEST, ST
胶原蛋白的病理破坏在影响人体各个器官系统的炎症性疾病状态的发展中起着关键作用。炎症部位的中性粒细胞可以通过释放一种金属酶（胶原酶）来潜在地降解胶原，胶原酶以一种潜伏的无活性形式储存。被触发的人中性粒细胞释放并同时激活其潜伏的胶原酶。潜伏酶的激活与氧化过程相结合，需要产生高活性氧代谢物次氯酸。潜在胶原酶活性的氧化调节在体内结缔组织损伤的发病机制中可能是重要的。
The pathological destruction of collagen plays a key role in the development of inflammatory disease states affecting every organ system in the human body. Neutrophils localized at inflammatory sites can potentially degrade collagen by releasing a metalloenzyme, collagenase, which is stored in a latent inactive form. Triggered human neutrophils were shown to release and simultaneously activate their latent collagenase. The activation of the latent enzyme was coupled to an oxidative process that required the generation of a highly reactive oxygen metabolite, hypochlorous acid. Oxidative regulation of latent collagenase activity may be important in the pathogenesis of connective tissue damage in vivo.