Stromelysin-1 and gelatinase A are upregulated before TNF-α in LPS-stimulated neuroinflammation
Stromelysin-1 and gelatinase A are upregulated before TNF-α in LPS-stimulated neuroinflammation
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DOI：
10.1016/s0006-8993(02)02303-x
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发表时间：
2002-04-12
期刊：
影响因子：
2.9
通讯作者：
Rosenberg, GA
中科院分区：
文献类型：
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作者：
Mun-Bryce, S;Lukes, A;Rosenberg, GA
神经炎症诱导复杂的分子级联反应，导致细胞蛋白水解。基质金属蛋白酶（MMPs）在许多神经炎性疾病中攻击细胞外基质的所有成分，并导致血脑屏障（BBB）的延迟开放。早些时候。我们发现脂多糖（LPS）通过明胶酶B （MMP-9）的作用破坏血脑屏障。在脑缺血的研究中，在星形细胞端足中发现明胶酶a (MMP-2)，在小胶质细胞中发现基质溶解素-1 （MMP-3）。由于其他MMPs可能在lps诱导的损伤中起重要作用，我们使用竞争性聚合酶链反应（PCR）和免疫组织化学方法研究了几种MMPs和炎症介质肿瘤坏死因子（tnf - α）的基因转录和细胞定位。与未注射lps的脑组织相比，注射lps后2小时脑组织中MMP-2和-3 mRNA水平显著升高(P
Neuroinflammation induces a complex molecular cascade that leads to the proteolysis of cells. Matrix metalloproteinases (MMPs) attack all components of the extracellular matrix in a number of neuroinflammatory diseases and cause a delayed opening of the blood-brain barrier (BBB). Earlier. we showed that lipopolysaccharide (LPS) disrupted the BBB through the action of gelatinase B (MMP-9). In a study of cerebral ischemia, gelatinase A (MMP-2) was seen in astrocytic end-feet and stromelysin-1 (MMP-3) in microglia. Since other MMPs may be important in LPS-induced injury, we studied the gene transcription and cellular localization of several MMPs and an inflammatory mediator, tumor necrosis factor (TNF-alpha), using competitive polymerase chain reaction (PCR) and immunohistochemical methods. Significantly elevated levels of MMP-2 and -3 mRNA were observed in LPS-injected brains by 2 h after injection as compared to non-injected brain tissue (P