A macrophage subpopulation promotes airineme-mediated intercellular communication in a matrix metalloproteinase-9 dependent manner.
A macrophage subpopulation promotes airineme-mediated intercellular communication in a matrix metalloproteinase-9 dependent manner.
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巨噬细胞亚群以基质金属蛋白酶-9依赖的方式促进航空素介导的细胞间通讯。
DOI:
10.1016/j.celrep.2023.112818
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发表时间:
2023-07-25
期刊:
影响因子:
8.8
通讯作者:
中科院分区:
文献类型:
--
作者:
Tissue-resident macrophages are heterogeneous and perform location-dependent functions. Skin resident macrophages play intriguing roles in long-distance intercellular signaling by mediating cellular protrusions called airinemes in zebrafish. These macrophages relay signaling molecules containing airineme vesicles between pigment cells, and their absence disrupts airineme-mediated signaling and pigment pattern formation. It is unknown if the same macrophages control both these signaling and typical immune functions or if a separate subpopulation functions in intercellular communication. With high-resolution imaging and genetic ablation approaches, we identify a macrophage subpopulation responsible for airineme-mediated signaling. These seem to be distinct from conventional skin-resident macrophages by their ameboid morphology and faster or expansive migratory behaviors. They resemble ectoderm-derived macrophages termed metaphocytes. Metaphocyte ablation markedly decreases airineme extension and signaling. In addition, these ameboid/metaphocytes require matrix metalloproteinase-9 for their migration and airineme-mediated signaling. These results reveal a macrophage subpopulation with specialized functions in airineme-mediated signaling, which may play roles in other aspects of intercellular communication. TRMs are highly heterogeneous and often perform non-immune functions. Bowman et al. discover that metaphocytes, an epithelial-derived macrophage subpopulation, are responsible for airinemes, a long, thin cellular protrusion required for intercellular signaling in zebrafish pigment pattern formation, and their role in airineme-mediated signaling depends on MMP9 activity.
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