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discs, mmp, fig, pubmed, undead, damage, hemocytes, ros, google, scholar, supplementary, cas, jnk, tumor, drosophila, cell, cells, data, hidp, activation, imaginal, side, basal, perlecan, activity, tissue, rnai, expression, control, overgrowth, central, nature, fluorescence, model, recruitment, sufficient, biol, macrophages, similar, eygal, disc, eye, hemocyte, damaged, neoplastic, aip, labeling, analyzed, salepv, intensity,

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nature portfolio privacy policy uas-dl uas-psq uas-lola/+ c-jun n-terminal kinase galphaq-phospholipase cbeta-ca2+ pathway advertising lgl4 frt40a/tub-gal80 frt40a frt42d vps25n55/frt42d tub-gal80 frt42d hpo42–47/frt42d tub-gal80 secreted nature research design research resources jose carlos pastor-pareja nature 439 nature escrt-ii component vps25 reprints ros-mediated post-translational activation ey-gal4 uas-p35/cyo author information authors 10 μg/ml dq-gelatin substrate undead ey-gal4-expressing portion yield m2-polarized tams2 quantitative real-time pcr eye-antennal imaginal disc open questions rabbit anti-cleaved dcp-1 apoptosis-induced compensatory proliferation massachusetts medical school peer review reactive oxygen species h2o2-treated eye discs fluorescein labeled dq-gelatin vectashield mounting media cell-type specific antigens permissions membrane-bound matrix metalloproteinase open 3 autophagy-mediated regeneration reporting summary apical-basal polarity rabbit anti-phospho jnk source data file dq-gelatin cleavage substrate scanning electron microscopy stress kinase jnk early larval lethality transmission electron microscopy peer reviewer reports jnk-mediated mmp2 upregulation

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      headline:Basement membrane damage by ROS- and JNK-mediated Mmp2 activation drives macrophage recruitment to overgrown tissue
      description:Macrophages are a major immune cell type infiltrating tumors and promoting tumor growth and metastasis. To elucidate the mechanism of macrophage recruitment, we utilize an overgrowth tumor model (“undead” model) in larval Drosophila imaginal discs that are attached by numerous macrophages. Here we report that changes to the microenvironment of the overgrown tissue are important for recruiting macrophages. First, we describe a correlation between generation of reactive oxygen species (ROS) and damage of the basement membrane (BM) in all neoplastic, but not hyperplastic, models examined. ROS and the stress kinase JNK mediate the accumulation of matrix metalloproteinase 2 (Mmp2), damaging the BM, which recruits macrophages to the tissue. We propose a model where macrophage recruitment to and activation at overgrowing tissue is a multi-step process requiring ROS- and JNK-mediated Mmp2 upregulation and BM damage. These findings have implications for understanding the role of the tumor microenvironment for macrophage activation. The molecular mechanisms regulating macrophage recruitment to tumors are unclear. Here, the authors use a Drosophila overgrowth model to show how damaged basement membranes recruit macrophages to undead tissue, via an interdependent effect of reactive oxygen species and matrix metalloproteinase 2.
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