Interleukin-33 promotes inflammation-induced lymphangiogenesis via ST2/TRAF6-mediated Akt/eNOS/NO signalling pathway.

ABSTRACT: The interplay between inflammation and lymphangiogenesis is mediated by various cytokines. However, most of these molecules and their associated mechanism are yet to be defined. Here, we explored the role of IL-33 in modulating inflammation-induced lymphangiogenesis (ILA) and its underlying mechanisms using an ILA mouse model and a lymphatic endothelial cell (LEC) line. Our results show that IL-33 promoted the proliferation, migration and tube formation of LECs and ILA in vivo. The pro-lymphangiogenic activity of IL-33 was abolished by ST2 blockage. In mechanisms, IL-33 induced the phosphorylation of Akt/eNOS to produce NO in LECs. The IL-33-induced Akt/eNOS activation was suppressed by the PI3K-specific-inhibitor wortmannin, and NO-production was inhibited by both wortmannin and the NO sy

SUBMITTER: Han L 

PROVIDER: S-EPMC5587532 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature