Markovic D S, Vinnakota K, Chirasani S, Synowitz M, Raguet H, Stock K, Sliwa M, Lehmann S, Kälin R, van Rooijen N, Holmbeck K, Heppner F L, Kiwit J, Matyash V, Lehnardt S, Kaminska B, Glass R, Kettenmann H
Cellular Neuroscience, Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany.
Proc Natl Acad Sci U S A. 2009 Jul 28;106(30):12530-5. doi: 10.1073/pnas.0804273106. Epub 2009 Jul 15.
Diffuse infiltration of glioma cells into normal brain tissue is considered to be a main reason for the unfavorable outcomes of patients with malignant gliomas. Invasion of glioma cells into the brain parenchyma is facilitated by metalloprotease-mediated degradation of the extracellular matrix. Metalloproteases are released as inactive pro-forms and get activated upon cleavage by membrane bound metalloproteases. Here, we show that membrane type 1 metalloprotease (MT1-MMP) is up-regulated in glioma-associated microglia, but not in the glioma cells. Overexpression of MT1-MMP is even lethal for glioma cells. Glioma-released factors trigger the expression and activity of MT1-MMP via microglial toll-like receptors and the p38 MAPK pathway, as deletion of the toll-like receptor adapter protein MyD88 or p38 inhibition prevented MT1-MMP expression and activity in cultured microglial cells. Microglial MT1-MMP in turn activates glioma-derived pro-MMP-2 and promotes glioma expansion, as shown in an ex vivo model using MT1-MMP-deficient brain tissue and a microglia depletion paradigm. Finally, MyD88 deficiency or microglia depletion largely attenuated glioma expansion in 2 independent in vivo models.
胶质瘤细胞向正常脑组织的弥漫性浸润被认为是恶性胶质瘤患者预后不良的主要原因。金属蛋白酶介导的细胞外基质降解促进了胶质瘤细胞向脑实质的侵袭。金属蛋白酶以无活性的前体形式释放,并在被膜结合金属蛋白酶切割后被激活。在此,我们表明1型膜金属蛋白酶(MT1-MMP)在胶质瘤相关小胶质细胞中上调,但在胶质瘤细胞中未上调。MT1-MMP的过表达甚至对胶质瘤细胞具有致死性。胶质瘤释放的因子通过小胶质细胞Toll样受体和p38丝裂原活化蛋白激酶(MAPK)途径触发MT1-MMP的表达和活性,因为Toll样受体衔接蛋白MyD88的缺失或p38抑制可阻止培养的小胶质细胞中MT1-MMP的表达和活性。如使用MT1-MMP缺陷脑组织和小胶质细胞耗竭范式的体外模型所示,小胶质细胞MT1-MMP反过来激活胶质瘤衍生的前基质金属蛋白酶-2并促进胶质瘤扩张。最后,在2个独立的体内模型中,MyD88缺陷或小胶质细胞耗竭在很大程度上减弱了胶质瘤的扩张。