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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Matrix metalloproteinase expression in an experimentally-induced DTH model of multiple sclerosis in the rat CNS.
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Matrix metalloproteinase expression in an experimentally-induced DTH model of multiple sclerosis in the rat CNS.

机译：大鼠中枢神经系统多发性硬化症的实验诱导DTH模型中基质金属蛋白酶的表达。

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摘要

In an experimentally-induced DTH model of MS, we examined mRNA and protein expression of a range of MMPs and of TNFalpha to establish the contribution that individual MMPs might make to the pathogenesis. In control rat brain, mRNA for all of the MMPs examined was detectable. However, by immunohistochemistry, only MMP-2 could be detected. In the DTH lesions, significant increases in the level of mRNA expression were observed for MMP-7, MMP-8, MMP-12, and TNFalpha. Where expression of MMP mRNA was increased, there was a corresponding increase in protein expression detected by immunohistochemistry. To determine whether the upregulated MMPs could invoke destructive events in the CNS, highly purified activated MMP-7, MMP-8, and MMP-9 were stereotaxically injected into the brain parenchyma. All provoked recruitment of leukocytes and BBB breakdown. In addition, MMPs 7 and 9 induced loss of myelin staining. In conclusion, specific MMPs are upregulated in DTH lesions; for the most part, measurement of mRNA was a predictor of increased protein expression. From our injections of MMPs, it is clear that the upregulated MMPs in the DTH lesions could participate in the disruption of the BBB, leukocyte recruitment, and tissue damage.
机译：在实验诱导的MS DTH模型中，我们检查了一系列MMP和TNFalpha的mRNA和蛋白表达，以确定单个MMP可能对发病的作用。在对照大鼠脑中，可检测到所有MMP的mRNA。但是，通过免疫组织化学只能检测到MMP-2。在DTH病变中，观察到MMP-7，MMP-8，MMP-12和TNFalpha的mRNA表达水平显着增加。 MMP mRNA的表达增加的地方，通过免疫组织化学检测到相应的蛋白质表达增加。为了确定上调的MMP是否会在CNS中引起破坏性事件，将高度纯化的活化MMP-7，MMP-8和MMP-9立体定位注射到脑实质中。所有这些都引起白细胞募集和血脑屏障破坏。此外，MMP 7和9导致髓磷脂染色的丧失。总之，DTH病变中特定的MMPs上调。在大多数情况下，mRNA的测量可预测蛋白质表达的增加。从我们注射的MMP中，很明显DTH病变中的MMP上调可能参与了BBB的破坏，白细胞募集和组织损伤。

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