Matrix metalloproteinase-9 and spontaneous hemorrhage in an animal model of cerebral amyloid angiopathy
Matrix metalloproteinase-9 and spontaneous hemorrhage in an animal model of cerebral amyloid angiopathy
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DOI：
10.1002/ana.10671
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发表时间：
2003-09-01
影响因子：
11.2
通讯作者：
Xu, J
中科院分区：
文献类型：
--
作者：
Lee, JM;Yin, KJ;Xu, J
我们研究了细胞外基质降解酶基质金属蛋白酶-9 （MMP-9）在脑淀粉样血管病（CAA）诱导的自发性出血发病机制中的潜在作用。淀粉样蛋白- β肽（Abeta）诱导小鼠脑内皮细胞中MMP-9的合成、释放和激活，导致细胞外基质降解增加。此外，在老年APPsw转基因小鼠的caa血管中观察到广泛的MMP-9免疫反应性，有微出血的证据，但在老年野生型和年轻APPsw小鼠中未检测到。这些结果提示，AP刺激血管中MMP-9表达的增加可能在CAA患者自发性脑出血的发病机制中起作用。
We examined the potential role of the extra-cellular matrix-degrading enzyme, matrix metalloproteinase-9 (MMP-9), in the pathogenesis of cerebral amyloid angiopathy (CAA)-induced spontaneous hemorrhage. The amyloid-beta peptide (Abeta) induced the synthesis, release and activation of MMP-9 in murine cerebral endothelial cells, resulting in increased extracellular matrix degradation. Furthermore, extensive MMP-9 immunoreactivity was observed in CAA-vessels with evidence of microhemorrhage in aged APPsw transgenic mice, but not detected in aged wild type or young APPsw mice. These results suggest that increased vascular MMP-9 expression, stimulated by AP, may play a role in the pathogenesis of spontaneous intracerebral hemorrhage in patients with CAA.