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- W2118974455 abstract "<h3>Rationale</h3> Successful recovery from acute lung injury requires inhibition of neutrophil influx and clearance of apoptotic neutrophils. However, the mechanisms underlying recovery remain unclear. <h3>Objectives</h3> We investigated the ameliorative effects of vascular endothelial growth factor receptor-3 (VEGFR-3)/VEGF-C signaling in macrophages in lipopolysaccharide-induced lung injury. <h3>Methods</h3> Lipopolysaccharides were intranasally injected into wild-type and transgenic mice. Gain- and loss- of VEGF-C/VEGFR-3 signaling function experiments employed adenovirus-mediated intranasal delivery of VEGF-C (Ad-VEGF-C vector) and soluble VEGFR-3, or, anti-VEGFR-3 blocking antibodies and mice with a deletion of VEGFR-3 in myeloid cells. <h3>Measurements and Main Results</h3> The early phase of lung injury was significantly alleviated by the overexpression of VEGF-C with increased levels of bronchoalveolar lavage fluid (BALF) interleukin (IL)-10, but worsened in the later phase by VEGFR-3 inhibition upon administration of Ad-sVEGFR-3 vector. Injection of anti-VEGFR-3 antibodies to the mice in the resolution phase inhibited recovery from lung injury. The VEGFR-3 deleted mice had a shorter survival time than littermates and more severe lung injury in the resolution phase. Alveolar macrophages in the resolution phase digested most of extrinsic apoptotic neutrophils, and VEGF-C/VEGFR-3 signaling increased efferocytosis <i>via</i> upregulation of integrin alpha v in the macrophages. We also found that incubation with BALF from acute respiratory distress syndrome (ARDS) patients, but not from controls, decreases VEGFR-3 expression and the efficiency of IL-10 expression and efferocytosis in human monocyte-derived macrophages. <h3>Conclusions</h3> VEGFR-3/VEGF-C signaling in macrophages ameliorates experimental lung injury. This mechanism may provide an explanation also for ARDS resolution." @default.
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- W2118974455 date "1997-07-01" @default.
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- W2118974455 title "Molecular Biology of Cancer" @default.
- W2118974455 doi "https://doi.org/10.1136/jmg.34.7.615" @default.
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