A 70-kDa amino-terminal fibronectin fragment supports gelatin binding to macrophages and decreases gelatinase activity.
A 70-kDa amino-terminal fibronectin fragment supports gelatin binding to macrophages and decreases gelatinase activity.
复制标题
70 kDa 氨基末端纤连蛋白片段支持明胶与巨噬细胞结合并降低明胶酶活性。
DOI：
10.1002/jlb.64.3.351
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发表时间：
1998
影响因子：
5.5
通讯作者：
Kaplan,JE
中科院分区：
文献类型：
--
作者：
Penc,SF;Blumenstock,FA;Kaplan,JE
我们以前报道过，通过将巨噬细胞与70-kDa氨基末端纤连蛋白片段和可溶性未标记明胶预孵育，可诱导巨噬细胞反应，增加与125 I-放射性标记的可溶性变性胶原（明胶）的结合[S. F. Penc，F. A. Blumenstock，J. E. 03 The Dog（1995）58，501-509]。我们现在报告说，这种反应既不需要蛋白质合成，也不需要细胞表面和内部之间受体的再循环。然而，用胰蛋白酶去除细胞表面成分表明，诱导明胶结合需要天然细胞表面成分。结果发现，在存在70 kDa纤连蛋白片段和明胶的情况下，细胞层中的基质金属蛋白酶-2（MMP-2）和基质金属蛋白酶-9（MMP-9）活性分别显著降低或检测不到。在用1 '10-菲咯啉抑制基质降解金属蛋白酶活性后，可以重现类似水平的明胶结合增加。这些结果表明，通过与70-kDa纤连蛋白片段和明胶的相互作用，启动了降低明胶酶活性和增加明胶结合的巨噬细胞特异性反应。64：351-357; 1998.
We previously reported that a macrophage response that increased binding to125I‐radiolabeled soluble denatured collagen (gelatin) was induced by preincubation of macrophage with a 70‐kDa amino‐terminal fibronectin fragment and soluble nonlabeled gelatin [S. F. Penc, F. A. Blumenstock, J. E. Kaplan (1995)J. Leukoc. Biol. 58, 501–509]. We now report that neither protein synthesis nor recycling of receptors between the cell surface and interior were required for this response. However, removal of cell surface components with trypsin demonstrated that induced gelatin binding required native cell surface constituents. It was found that in the presence of the 70‐kDa fibronectin fragment and gelatin, matrix metalloprotease‐2 (MMP‐2) and matrix metalloprotease‐9 (MMP‐9) activity in the cell layers was significantly decreased or undetectable, respectively. Similar levels of increased gelatin binding could be reproduced after inhibition of matrix‐degrading metalloprotease activity with 1'10‐phenanthroline. These results demonstrate that a macrophage specific response that decreased gelatinase activity and increased gelatin binding was initiated by interaction with a 70‐kDa fibronectin fragment and gelatin.J. Leukoc. Biol. 64: 351–357; 1998.