Diverse roles of matrix metalloproteinases and tissue inhibitors of metalloproteinases in neuroinflammation and cerebral ischemia.

摘要: Regulation of the extracellular matrix by proteases and protease inhibitors is a fundamental biological process for normal growth, development repair in CNS. Matrix metalloproteinases (MMPs) tissue (TIMPs) are major extracellular-degrading enzymes. Two other enzyme families, disintegrin metalloproteinase (ADAM), serine proteases, plasminogen/plasminogen activator (P/PA) system, also involved degradation. Normally, highly integrated action these families remodels all components performs essential functions at cell surface signaling, survival, death. During inflammatory response induced infection, autoimmune reactions hypoxia/ischemia, abnormal expression activation lead to breakdown matrix, resulting opening blood-brain barrier (BBB), preventing eventually leading There several key MMPs ADAMs that have been implicated neuroinflammation: gelatinases A B (MMP-2 -9), stromelysin-1 (MMP-3), membrane-type MMP (MT1-MMP or MMP-14), tumor necrosis factor-alpha converting (TACE). In addition, TIMP-3, which bound surface, promotes death impedes angiogenesis. Inhibitors available, but balancing beneficial detrimental effects agents remains challenge.