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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Pericellular mobilization of the tissue-destructive cysteine proteinases, cathepsins B, L, and S, by human monocyte-derived macrophages.
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Pericellular mobilization of the tissue-destructive cysteine proteinases, cathepsins B, L, and S, by human monocyte-derived macrophages.

机译：人单核细胞衍生的巨噬细胞对组织破坏性半胱氨酸蛋白酶，组织蛋白酶B，L和S的细胞周围动员。

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摘要

Human macrophages are believed to damage host tissues in chronic inflammatory disease states, but these cells have been reported to express only modest degradative activity in vitro. However, while examining the ability of human monocytes to degrade the extracellular matrix component elastin, we identified culture conditions under which the cells matured into a macrophage population that displayed a degradative phenotype hundreds of times more destructive than that previously ascribed to any other cell population. The monocyte-derived macrophages synthesized elastinolytic matrix metalloproteinases (i.e., gelatinase B and matrilysin) as well as cysteine proteinases (i.e., cathepsins B, L, and S), but only the cathepsins were detected in the extracellular milieu as fully processed, mature enzymes by either vital fluorescence or active-site labeling. Consistent with these observations, macrophage-mediated elastinolytic activity was not affected by matrix metalloproteinase inhibitors but could be almost completely abrogated by inhibiting cathepsins L and S. These data demonstrate that human macrophages mobilize cysteine proteinases to arm themselves with a powerful effector mechanism that can participate in the pathophysiologic remodeling of the extracellular matrix.
机译：据信人类巨噬细胞在慢性炎症疾病状态下损害宿主组织，但是据报道这些细胞在体外仅表达适度的降解活性。但是，在检查人单核细胞降解细胞外基质成分弹性蛋白的能力时，我们确定了培养条件，在这些条件下，细胞成熟为巨噬细胞群，其表现出的破坏性表型比先前归因于任何其他细胞群体的破坏性高数百倍。单核细胞衍生的巨噬细胞合成了弹性蛋白酶基质金属蛋白酶（即明胶酶B和基质溶素）以及半胱氨酸蛋白酶（即组织蛋白酶B，L和S），但只有胞蛋白酶在细胞外环境中被检测为完全加工的成熟酶。通过重要的荧光或活性部位标记。与这些观察结果一致，巨噬细胞介导的弹性蛋白酶分解活性不受基质金属蛋白酶抑制剂的影响，但可以通过抑制组织蛋白酶L和S几乎被完全消除。这些数据表明，人类巨噬细胞动员半胱氨酸蛋白酶以强大的效应子机制武装自己，可以参与其中在细胞外基质的病理生理重塑中的作用。

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