Expression and activation of matrix metalloproteinase-2 and-9 in rat brain after transient focal cerebral ischemia
Expression and activation of matrix metalloproteinase-2 and-9 in rat brain after transient focal cerebral ischemia
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DOI：
10.1006/nbdi.2001.0435
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发表时间：
2001-10-01
影响因子：
6.1
通讯作者：
Justicia, C
中科院分区：
文献类型：
--
作者：
Planas, AM;Solé, S;Justicia, C
基质金属蛋白酶（MMPs）降解细胞外基质，并在发育过程中和损伤后发挥关键作用。采用酶谱、免疫印迹和免疫组织化学方法，对大鼠脑缺血后MMP-2（明胶酶A）和MMP-9（明胶酶B）的表达进行了研究。对照组大鼠脑显示组成型MMP-2，并在较小程度上，MMP-9，这主要是作为酶原存在。MMP-2蛋白位于神经元、胶质细胞和内皮细胞的细胞体中，而MMP-9与神经元和有髓纤维束相关。缺血在两个时间波中大大增加MMP活化，在第一个时间波中，MMP-9蛋白从4 h至4d被诱导，并且在4 h检测到MMP-2的小而短暂的增加。第二波显示到第4天MMP-2蛋白表达和活化的大量增加，这与反应性小胶质细胞/巨噬细胞中丰富的MMP-2相容。我们的研究结果与缺血后不久可能在神经元中MMP-9前体的渐进诱导相一致。对于MMP-2，结果表明再灌注后立即离散生产，而MMP-2的表达和活化非常增强，归因于小胶质细胞/巨噬细胞发生在第4天，它可能有助于这些反应性细胞的吞噬作用。(C)北京：科学出版社.
Matrix metalloproteinases (MMPs) degrade the extracellular matrix and carry out key functions during development and after injury. By means of zymography, Western blot and immunohistochemistry, we studied MMP-2 (gelatinase A) and MMP-9 (gelatinase B) in rat brain after focal cerebral ischemia. The control rat brain showed constitutive MMP-2 and, to a lesser extent, MMP-9, which were mainly present as prozymogens. MMP-2 protein was located in the cell body of neurons, glia, and endothelium, whereas MMP-9 was associated to neurons and myelinated fibre tracts. Ischemia greatly increased MMP activation in two temporal waves, in the first one, MMP-9 protein was induced from 4 h to 4 days, and also a small and short-lasting increase in MMP-2 was detected at 4 h. The second wave showed a massive increase in MMP-2 protein expression and activation by day 4, which was compatible with abundant MMP-2 in reactive microglia/macrophages. Our results are compatible with progressive induction of MMP-9 proform, likely in neurons, shortly after ischemia. For MMP-2, the results suggest a discrete production immediately after reperfusion, while a very enhanced expression and activation of MMP-2 attributable to microglia/macrophages occurs on day 4, and it might contribute to the phagocytic action of these reactive cells. (C) 2001 Academic Press.